- About
- Home
- Introduction
- Statistics
- Programs
- Dignet
- Gene
- GenePair
- BioSummarAI
- Help & Docs
- Documents
- Help
- FAQs
- Links
- Acknowledge
- Disclaimer
- Contact Us
Gene Information
Gene symbol: NPHS2
Gene name: nephrosis 2, idiopathic, steroid-resistant (podocin)
HGNC ID: 13394
Synonyms: SRN1, PDCN
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 10742096 | NPHS2 is almost exclusively expressed in the podocytes of fetal and mature kidney glomeruli, and encodes a new integral membrane protein, podocin, belonging to the stomatin protein family. |
| 2 | 11458036 | However, more recent studies on nephrin, a key component of the slit diaphragm, as well as the podocyte and slit diaphragm-associated intracellular proteins, CD2-associated protein, podocin and alpha-actinin-4, have emphasized the role of the slit diaphragm as a central size-selective filtration barrier. |
| 3 | 11562357 | Interaction with podocin facilitates nephrin signaling. |
| 4 | 11562357 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 5 | 11562357 | In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes. |
| 6 | 11562357 | Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. |
| 7 | 11562357 | Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria. |
| 8 | 11562357 | Interaction with podocin facilitates nephrin signaling. |
| 9 | 11562357 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 10 | 11562357 | In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes. |
| 11 | 11562357 | Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. |
| 12 | 11562357 | Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria. |
| 13 | 11562357 | Interaction with podocin facilitates nephrin signaling. |
| 14 | 11562357 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 15 | 11562357 | In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes. |
| 16 | 11562357 | Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. |
| 17 | 11562357 | Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria. |
| 18 | 11562357 | Interaction with podocin facilitates nephrin signaling. |
| 19 | 11562357 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 20 | 11562357 | In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes. |
| 21 | 11562357 | Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. |
| 22 | 11562357 | Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria. |
| 23 | 11701993 | The identification of nephrin, a component of the slit diaphragm, and the intracellular slit diaphragm associated proteins CD2AP and podocin has demonstrated the existence of proteins that directly contribute to a functional kidney filter. |
| 24 | 11730159 | In addition to nephrin, other podocyte proteins (podocin, alpha-actinin-4, CD2AP, FAT) have recently been identified and associated with the development of proteinuria. |
| 25 | 11733557 | Its product, podocin, is a new member of the stomatin family, which consists of hairpin-like integral membrane proteins with intracellular NH(2)- and COOH-termini. |
| 26 | 11733557 | Moreover, GST pull-down experiments reveal that podocin associates via its COOH-terminal domain with CD2AP, a cytoplasmic binding partner of nephrin, and with nephrin itself. |
| 27 | 11733557 | That podocin interacts with CD2AP and nephrin in vivo is shown by coimmunoprecipitation of these proteins from glomerular extracts. |
| 28 | 11733557 | Hence, as with the erythrocyte lipid raft protein stomatin, podocin is present in high-order oligomers and may serve a scaffolding function. |
| 29 | 11733557 | Its product, podocin, is a new member of the stomatin family, which consists of hairpin-like integral membrane proteins with intracellular NH(2)- and COOH-termini. |
| 30 | 11733557 | Moreover, GST pull-down experiments reveal that podocin associates via its COOH-terminal domain with CD2AP, a cytoplasmic binding partner of nephrin, and with nephrin itself. |
| 31 | 11733557 | That podocin interacts with CD2AP and nephrin in vivo is shown by coimmunoprecipitation of these proteins from glomerular extracts. |
| 32 | 11733557 | Hence, as with the erythrocyte lipid raft protein stomatin, podocin is present in high-order oligomers and may serve a scaffolding function. |
| 33 | 11733557 | Its product, podocin, is a new member of the stomatin family, which consists of hairpin-like integral membrane proteins with intracellular NH(2)- and COOH-termini. |
| 34 | 11733557 | Moreover, GST pull-down experiments reveal that podocin associates via its COOH-terminal domain with CD2AP, a cytoplasmic binding partner of nephrin, and with nephrin itself. |
| 35 | 11733557 | That podocin interacts with CD2AP and nephrin in vivo is shown by coimmunoprecipitation of these proteins from glomerular extracts. |
| 36 | 11733557 | Hence, as with the erythrocyte lipid raft protein stomatin, podocin is present in high-order oligomers and may serve a scaffolding function. |
| 37 | 11733557 | Its product, podocin, is a new member of the stomatin family, which consists of hairpin-like integral membrane proteins with intracellular NH(2)- and COOH-termini. |
| 38 | 11733557 | Moreover, GST pull-down experiments reveal that podocin associates via its COOH-terminal domain with CD2AP, a cytoplasmic binding partner of nephrin, and with nephrin itself. |
| 39 | 11733557 | That podocin interacts with CD2AP and nephrin in vivo is shown by coimmunoprecipitation of these proteins from glomerular extracts. |
| 40 | 11733557 | Hence, as with the erythrocyte lipid raft protein stomatin, podocin is present in high-order oligomers and may serve a scaffolding function. |
| 41 | 11786407 | Given its similarity with the stomatin family proteins, podocin is predicted to be an integral membrane protein with a single membrane domain forming a hairpin-like structure placing both N- and C-termini in the cytosol. |
| 42 | 11793093 | Mutations in podocyte proteins, such as nephrin, alpha-actinin 4, and podocin, are associated with proteinuria and nephrotic syndrome. |
| 43 | 11793093 | We postulated that in Galloway-Mowat syndrome the mutation would be in a protein that is expressed both in podocytes and neurons, such as synaptopodin, GLEPP1, or nephrin. |
| 44 | 11793093 | We therefore analyzed kidney tissue from normal children (n=3), children with congenital nephrotic syndrome of the Finnish type (CNF, n=3), minimal change disease (MCD, n=3), focal segmental glomerulosclerosis (FSGS, n=3), and Galloway-Mowat syndrome (n=4) by immunohistochemistry for expression of synaptopodin, GLEPP1, intracellular domain of nephrin (nephrin-I), and extracellular domain of nephrin (nephrin-E). |
| 45 | 11793093 | Synaptopodin, GLEPP1, and nephrin were strongly expressed in normal kidney tissue. |
| 46 | 11793093 | Nephrin was absent, and synaptopodin and GLEPP1 expression were decreased in CNF. |
| 47 | 11793093 | The expression of all three proteins was reduced in MCD and FSGS; the decrease in expression being more marked in FSGS. |
| 48 | 11793093 | Synaptopodin, GLEPP1, and nephrin expression was present, although reduced in Galloway-Mowat syndrome. |
| 49 | 11793093 | We conclude that the reduced expression of synaptopodin, GLEPP1, and nephrin in Galloway- Mowat syndrome is a secondary phenomenon related to the proteinuria, and hence synaptopodin, GLEPP1, and nephrin are probably not the proteins mutated in Galloway-Mowat syndrome. |
| 50 | 11856766 | A conditionally immortalized human podocyte cell line demonstrating nephrin and podocin expression. |
| 51 | 11856766 | After transfer to the "nonpermissive" temperature (37 degrees C), they entered growth arrest and expressed markers of differentiated in vivo podocytes, including the novel podocyte proteins, nephrin, podocin, CD2AP, and synaptopodin, and known molecules of the slit diaphragm ZO-1, alpha-, beta-, and gamma-catenin and P-cadherin. |
| 52 | 11856766 | The differentiation was accompanied by a growth arrest and the upregulation of cyclin-dependent kinase inhibitors, p27 and p57, as well as cyclin D(1), whereas cyclin A was downregulated. |
| 53 | 11856766 | A conditionally immortalized human podocyte cell line demonstrating nephrin and podocin expression. |
| 54 | 11856766 | After transfer to the "nonpermissive" temperature (37 degrees C), they entered growth arrest and expressed markers of differentiated in vivo podocytes, including the novel podocyte proteins, nephrin, podocin, CD2AP, and synaptopodin, and known molecules of the slit diaphragm ZO-1, alpha-, beta-, and gamma-catenin and P-cadherin. |
| 55 | 11856766 | The differentiation was accompanied by a growth arrest and the upregulation of cyclin-dependent kinase inhibitors, p27 and p57, as well as cyclin D(1), whereas cyclin A was downregulated. |
| 56 | 11956244 | LMX1B encodes a LIM-homeodomain transcription factor. |
| 57 | 11956244 | Using antibodies to podocyte proteins important for podocyte function, we found that Lmx1b(-/-) podocytes express near-normal levels of nephrin, synaptopodin, ZO-1, alpha3 integrin, and GBM laminins. |
| 58 | 11956244 | However, mRNA and protein levels for CD2AP and podocin were greatly reduced, suggesting a cooperative role for these molecules in foot process and slit diaphragm formation. |
| 59 | 11956244 | We identified several LMX1B binding sites in the putative regulatory regions of both CD2AP and NPHS2 (podocin) and demonstrated that LMX1B binds to these sequences in vitro and can activate transcription through them in cotransfection assays. |
| 60 | 11956244 | LMX1B encodes a LIM-homeodomain transcription factor. |
| 61 | 11956244 | Using antibodies to podocyte proteins important for podocyte function, we found that Lmx1b(-/-) podocytes express near-normal levels of nephrin, synaptopodin, ZO-1, alpha3 integrin, and GBM laminins. |
| 62 | 11956244 | However, mRNA and protein levels for CD2AP and podocin were greatly reduced, suggesting a cooperative role for these molecules in foot process and slit diaphragm formation. |
| 63 | 11956244 | We identified several LMX1B binding sites in the putative regulatory regions of both CD2AP and NPHS2 (podocin) and demonstrated that LMX1B binds to these sequences in vitro and can activate transcription through them in cotransfection assays. |
| 64 | 11956245 | The LIM-homeodomain transcription factor Lmx1b plays a crucial role in podocytes. |
| 65 | 11956245 | Expression of the alpha4 chain of collagen IV and of podocin was also severely reduced. |
| 66 | 11956245 | Using gel shift assays, we demonstrated that LMX1B bound to two AT-rich sequences in the promoter region of NPHS2, the gene encoding podocin. |
| 67 | 11956245 | Our results demonstrate that Lmx1b regulates important steps in glomerular development and establish a link between three hereditary kidney diseases: nail-patella syndrome (Lmx1b), steroid-resistant nephrotic syndrome (podocin), and Alport syndrome (collagen IV alpha4). |
| 68 | 11956245 | The LIM-homeodomain transcription factor Lmx1b plays a crucial role in podocytes. |
| 69 | 11956245 | Expression of the alpha4 chain of collagen IV and of podocin was also severely reduced. |
| 70 | 11956245 | Using gel shift assays, we demonstrated that LMX1B bound to two AT-rich sequences in the promoter region of NPHS2, the gene encoding podocin. |
| 71 | 11956245 | Our results demonstrate that Lmx1b regulates important steps in glomerular development and establish a link between three hereditary kidney diseases: nail-patella syndrome (Lmx1b), steroid-resistant nephrotic syndrome (podocin), and Alport syndrome (collagen IV alpha4). |
| 72 | 11956245 | The LIM-homeodomain transcription factor Lmx1b plays a crucial role in podocytes. |
| 73 | 11956245 | Expression of the alpha4 chain of collagen IV and of podocin was also severely reduced. |
| 74 | 11956245 | Using gel shift assays, we demonstrated that LMX1B bound to two AT-rich sequences in the promoter region of NPHS2, the gene encoding podocin. |
| 75 | 11956245 | Our results demonstrate that Lmx1b regulates important steps in glomerular development and establish a link between three hereditary kidney diseases: nail-patella syndrome (Lmx1b), steroid-resistant nephrotic syndrome (podocin), and Alport syndrome (collagen IV alpha4). |
| 76 | 12065681 | The molecules studied included the filtration slit component nephrin, the hairpin-like membrane protein podocin, the basolateral adhesion molecules beta1 integrin and alpha-dystroglycan, and the cytoskeleton-linking intermediary beta-catenin and the actin-associated alpha-actinin-4. |
| 77 | 12065681 | The results showed diminished protein levels of podocin and nephrin in the PA-treated group. beta-catenin showed distinct down-regulation at 3 days of induction, and the control level was reached at 10 days. beta1 integrin was markedly up-regulated during induction. alpha-actinin-4 was not changed at the studied time points. |
| 78 | 12065681 | The molecules studied included the filtration slit component nephrin, the hairpin-like membrane protein podocin, the basolateral adhesion molecules beta1 integrin and alpha-dystroglycan, and the cytoskeleton-linking intermediary beta-catenin and the actin-associated alpha-actinin-4. |
| 79 | 12065681 | The results showed diminished protein levels of podocin and nephrin in the PA-treated group. beta-catenin showed distinct down-regulation at 3 days of induction, and the control level was reached at 10 days. beta1 integrin was markedly up-regulated during induction. alpha-actinin-4 was not changed at the studied time points. |
| 80 | 12217315 | The levels of Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome (NPHS2), and Nephrin, the gene mutated in congenital nephrotic syndrome of the Finnish type (NPHS1), are slightly reduced in kr(enu)/kr(enu) podocytes. |
| 81 | 12368218 | Co-localization of nephrin, podocin, and the actin cytoskeleton: evidence for a role in podocyte foot process formation. |
| 82 | 12368218 | The discovery of the genes for nephrin and podocin, which are mutated in two types of congenital nephrotic syndrome, was pivotal in establishing the podocyte as the central component of the glomerular filtration barrier. |
| 83 | 12368218 | In addition to membrane expression, nephrin and podocin were detected intracellularly in a filamentous pattern. |
| 84 | 12368218 | Double immunolabeling and depolymerization studies showed that nephrin and podocin partially co-localize with actin, most strikingly seen protruding from the tips of actin filaments, and are dependent on intact actin polymers for their intracellular distribution. |
| 85 | 12368218 | We demonstrate an intimate relationship between nephrin podocin and filamentous actin, and reason that disruption of nephrin/podocin could be a final common pathway leading to foot process effacement in proteinuric diseases. |
| 86 | 12368218 | Co-localization of nephrin, podocin, and the actin cytoskeleton: evidence for a role in podocyte foot process formation. |
| 87 | 12368218 | The discovery of the genes for nephrin and podocin, which are mutated in two types of congenital nephrotic syndrome, was pivotal in establishing the podocyte as the central component of the glomerular filtration barrier. |
| 88 | 12368218 | In addition to membrane expression, nephrin and podocin were detected intracellularly in a filamentous pattern. |
| 89 | 12368218 | Double immunolabeling and depolymerization studies showed that nephrin and podocin partially co-localize with actin, most strikingly seen protruding from the tips of actin filaments, and are dependent on intact actin polymers for their intracellular distribution. |
| 90 | 12368218 | We demonstrate an intimate relationship between nephrin podocin and filamentous actin, and reason that disruption of nephrin/podocin could be a final common pathway leading to foot process effacement in proteinuric diseases. |
| 91 | 12368218 | Co-localization of nephrin, podocin, and the actin cytoskeleton: evidence for a role in podocyte foot process formation. |
| 92 | 12368218 | The discovery of the genes for nephrin and podocin, which are mutated in two types of congenital nephrotic syndrome, was pivotal in establishing the podocyte as the central component of the glomerular filtration barrier. |
| 93 | 12368218 | In addition to membrane expression, nephrin and podocin were detected intracellularly in a filamentous pattern. |
| 94 | 12368218 | Double immunolabeling and depolymerization studies showed that nephrin and podocin partially co-localize with actin, most strikingly seen protruding from the tips of actin filaments, and are dependent on intact actin polymers for their intracellular distribution. |
| 95 | 12368218 | We demonstrate an intimate relationship between nephrin podocin and filamentous actin, and reason that disruption of nephrin/podocin could be a final common pathway leading to foot process effacement in proteinuric diseases. |
| 96 | 12368218 | Co-localization of nephrin, podocin, and the actin cytoskeleton: evidence for a role in podocyte foot process formation. |
| 97 | 12368218 | The discovery of the genes for nephrin and podocin, which are mutated in two types of congenital nephrotic syndrome, was pivotal in establishing the podocyte as the central component of the glomerular filtration barrier. |
| 98 | 12368218 | In addition to membrane expression, nephrin and podocin were detected intracellularly in a filamentous pattern. |
| 99 | 12368218 | Double immunolabeling and depolymerization studies showed that nephrin and podocin partially co-localize with actin, most strikingly seen protruding from the tips of actin filaments, and are dependent on intact actin polymers for their intracellular distribution. |
| 100 | 12368218 | We demonstrate an intimate relationship between nephrin podocin and filamentous actin, and reason that disruption of nephrin/podocin could be a final common pathway leading to foot process effacement in proteinuric diseases. |
| 101 | 12368218 | Co-localization of nephrin, podocin, and the actin cytoskeleton: evidence for a role in podocyte foot process formation. |
| 102 | 12368218 | The discovery of the genes for nephrin and podocin, which are mutated in two types of congenital nephrotic syndrome, was pivotal in establishing the podocyte as the central component of the glomerular filtration barrier. |
| 103 | 12368218 | In addition to membrane expression, nephrin and podocin were detected intracellularly in a filamentous pattern. |
| 104 | 12368218 | Double immunolabeling and depolymerization studies showed that nephrin and podocin partially co-localize with actin, most strikingly seen protruding from the tips of actin filaments, and are dependent on intact actin polymers for their intracellular distribution. |
| 105 | 12368218 | We demonstrate an intimate relationship between nephrin podocin and filamentous actin, and reason that disruption of nephrin/podocin could be a final common pathway leading to foot process effacement in proteinuric diseases. |
| 106 | 12397033 | Caveolin-1 co-immunoprecipitated with the podocyte slit diaphragm proteins nephrin and CD2AP, and dual immunofluorescence confirmed co-localization of caveolin-1 and nephrin. |
| 107 | 12397033 | Nevertheless, in caveolin-1-deficient mice, podocyte ultrastructure appeared normal, and the podocyte proteins synaptopodin, nephrin, and podocin were expressed normally. |
| 108 | 12424224 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 109 | 12424224 | Podocin interacts with the C-terminal domain of nephrin and facilitates nephrin-dependent signaling. |
| 110 | 12424224 | NEPH1 triggers AP-1 activation similarly to nephrin but requires the presence of Tec family kinases for efficient transactivation. |
| 111 | 12424224 | We conclude that NEPH1 defines a new family of podocin-binding molecules that are potential candidates for hereditary nephrotic syndromes not linked to either NPHS1 or NPHS2. |
| 112 | 12424224 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 113 | 12424224 | Podocin interacts with the C-terminal domain of nephrin and facilitates nephrin-dependent signaling. |
| 114 | 12424224 | NEPH1 triggers AP-1 activation similarly to nephrin but requires the presence of Tec family kinases for efficient transactivation. |
| 115 | 12424224 | We conclude that NEPH1 defines a new family of podocin-binding molecules that are potential candidates for hereditary nephrotic syndromes not linked to either NPHS1 or NPHS2. |
| 116 | 12424224 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 117 | 12424224 | Podocin interacts with the C-terminal domain of nephrin and facilitates nephrin-dependent signaling. |
| 118 | 12424224 | NEPH1 triggers AP-1 activation similarly to nephrin but requires the presence of Tec family kinases for efficient transactivation. |
| 119 | 12424224 | We conclude that NEPH1 defines a new family of podocin-binding molecules that are potential candidates for hereditary nephrotic syndromes not linked to either NPHS1 or NPHS2. |
| 120 | 12506137 | A rat homologue of podocin was cloned, and the expression of podocin was investigated and then compared with the nephrin and the ZO-1 expressions in rat experimental proteinuric models and in developing glomeruli. |
| 121 | 12506137 | The localization of podocin has close proximity to that of nephrin in normal adult rat glomeruli. |
| 122 | 12506137 | Podocin staining was restricted to the basal side of the podocyte of the early developing stage, whereas nephrin staining was detected on the basolateral surface of podocyte. |
| 123 | 12506137 | The redistribution of podocin was observed in the anti-nephrin antibody (ANA)-induced nephropathy and puromycin aminonucleoside (PAN) nephropathy. |
| 124 | 12506137 | The redistribution of podocin paralleled with nephrin in ANA nephropathy but not in PAN nephropathy. |
| 125 | 12506137 | A rat homologue of podocin was cloned, and the expression of podocin was investigated and then compared with the nephrin and the ZO-1 expressions in rat experimental proteinuric models and in developing glomeruli. |
| 126 | 12506137 | The localization of podocin has close proximity to that of nephrin in normal adult rat glomeruli. |
| 127 | 12506137 | Podocin staining was restricted to the basal side of the podocyte of the early developing stage, whereas nephrin staining was detected on the basolateral surface of podocyte. |
| 128 | 12506137 | The redistribution of podocin was observed in the anti-nephrin antibody (ANA)-induced nephropathy and puromycin aminonucleoside (PAN) nephropathy. |
| 129 | 12506137 | The redistribution of podocin paralleled with nephrin in ANA nephropathy but not in PAN nephropathy. |
| 130 | 12506137 | A rat homologue of podocin was cloned, and the expression of podocin was investigated and then compared with the nephrin and the ZO-1 expressions in rat experimental proteinuric models and in developing glomeruli. |
| 131 | 12506137 | The localization of podocin has close proximity to that of nephrin in normal adult rat glomeruli. |
| 132 | 12506137 | Podocin staining was restricted to the basal side of the podocyte of the early developing stage, whereas nephrin staining was detected on the basolateral surface of podocyte. |
| 133 | 12506137 | The redistribution of podocin was observed in the anti-nephrin antibody (ANA)-induced nephropathy and puromycin aminonucleoside (PAN) nephropathy. |
| 134 | 12506137 | The redistribution of podocin paralleled with nephrin in ANA nephropathy but not in PAN nephropathy. |
| 135 | 12506137 | A rat homologue of podocin was cloned, and the expression of podocin was investigated and then compared with the nephrin and the ZO-1 expressions in rat experimental proteinuric models and in developing glomeruli. |
| 136 | 12506137 | The localization of podocin has close proximity to that of nephrin in normal adult rat glomeruli. |
| 137 | 12506137 | Podocin staining was restricted to the basal side of the podocyte of the early developing stage, whereas nephrin staining was detected on the basolateral surface of podocyte. |
| 138 | 12506137 | The redistribution of podocin was observed in the anti-nephrin antibody (ANA)-induced nephropathy and puromycin aminonucleoside (PAN) nephropathy. |
| 139 | 12506137 | The redistribution of podocin paralleled with nephrin in ANA nephropathy but not in PAN nephropathy. |
| 140 | 12506137 | A rat homologue of podocin was cloned, and the expression of podocin was investigated and then compared with the nephrin and the ZO-1 expressions in rat experimental proteinuric models and in developing glomeruli. |
| 141 | 12506137 | The localization of podocin has close proximity to that of nephrin in normal adult rat glomeruli. |
| 142 | 12506137 | Podocin staining was restricted to the basal side of the podocyte of the early developing stage, whereas nephrin staining was detected on the basolateral surface of podocyte. |
| 143 | 12506137 | The redistribution of podocin was observed in the anti-nephrin antibody (ANA)-induced nephropathy and puromycin aminonucleoside (PAN) nephropathy. |
| 144 | 12506137 | The redistribution of podocin paralleled with nephrin in ANA nephropathy but not in PAN nephropathy. |
| 145 | 12619708 | Recently, identification of the mutated genes for some podocyte proteins (nephrin, podocin, alpha-actinin-4) in rare familial forms of nephrotic syndrome shed has new light on the molecular mechanisms of glomerular permselectivity. |
| 146 | 12646566 | Like Nephrin and Podocin, Neph1 was enriched in Triton X-100 detergent-resistant membrane fractions. |
| 147 | 12688182 | Mutation of the basic structural protein of slit diaphragm, nephrin, results in the Finnish type of the congenital nephrotic syndrome, mutations of other podocyte proteins, e.g. podocin, or alpha-actinin-4 result in congenital focal segmental glomerulosclerosis. |
| 148 | 12688182 | New information about the role of cubilin and megalin in the reabsorption of filtered albumin in the proximal tubule may contribute to the elucidation of the mechanisms of the tubulotoxicity of proteinuria; inhibition of albumin reabsorption in nephrotic subjects could lower the risk of interstitial fibrosis and progressive renal insufficiency. |
| 149 | 12704574 | Mutations in both podocin gene (NPHS2) alleles lead to a wide range of human disease, from childhood-onset steroid-resistant FSGS and minimal change disease to adult-onset FSGS. |
| 150 | 12761234 | The importance of several of them (nephrin, podocin, CD2AP, and Neph1) in the maintenance of the glomerular filtration barrier has been demonstrated by the occurrence of massive proteinuria when they are defective. |
| 151 | 12819019 | NPS is inherited as an autosomal dominant trait and caused by heterozygous loss of function mutations in LMX1B, a member of the LIM homeodomain protein family. |
| 152 | 12819019 | Strong reduction in the glomerular expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, two podocyte proteins critical for glomerular function, has been observed in Lmx1b null mice. |
| 153 | 12819019 | The glomerular basement membrane fibrillar material was specifically labeled with anti-type III collagen antibodies, suggesting a possible regulation of type III collagen expression by LMX1B. |
| 154 | 12819019 | The expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, was found to be normal in the seven patients. |
| 155 | 12819019 | These findings indicate that heterozygous mutations of LMX1B do not appear to dramatically affect the expression of type IV collagen chains, podocin, or CD2AP in NPS patients. |
| 156 | 12819019 | NPS is inherited as an autosomal dominant trait and caused by heterozygous loss of function mutations in LMX1B, a member of the LIM homeodomain protein family. |
| 157 | 12819019 | Strong reduction in the glomerular expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, two podocyte proteins critical for glomerular function, has been observed in Lmx1b null mice. |
| 158 | 12819019 | The glomerular basement membrane fibrillar material was specifically labeled with anti-type III collagen antibodies, suggesting a possible regulation of type III collagen expression by LMX1B. |
| 159 | 12819019 | The expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, was found to be normal in the seven patients. |
| 160 | 12819019 | These findings indicate that heterozygous mutations of LMX1B do not appear to dramatically affect the expression of type IV collagen chains, podocin, or CD2AP in NPS patients. |
| 161 | 12819019 | NPS is inherited as an autosomal dominant trait and caused by heterozygous loss of function mutations in LMX1B, a member of the LIM homeodomain protein family. |
| 162 | 12819019 | Strong reduction in the glomerular expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, two podocyte proteins critical for glomerular function, has been observed in Lmx1b null mice. |
| 163 | 12819019 | The glomerular basement membrane fibrillar material was specifically labeled with anti-type III collagen antibodies, suggesting a possible regulation of type III collagen expression by LMX1B. |
| 164 | 12819019 | The expression of the alpha3 and alpha4 chains of type IV collagen, and of podocin and CD2AP, was found to be normal in the seven patients. |
| 165 | 12819019 | These findings indicate that heterozygous mutations of LMX1B do not appear to dramatically affect the expression of type IV collagen chains, podocin, or CD2AP in NPS patients. |
| 166 | 12832477 | Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. |
| 167 | 12832477 | Mutations of NPHS1 or NPHS2, the genes encoding nephrin and podocin, as well as the targeted disruption of CD2-associated protein (CD2AP), lead to heavy proteinuria, suggesting that all three proteins are essential for the integrity of glomerular podocytes, the visceral glomerular epithelial cells of the kidney. |
| 168 | 12832477 | We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate PI3K-dependent AKT signaling in podocytes. |
| 169 | 12832477 | Using two-dimensional gel analysis in combination with a phosphoserine-specific antiserum, we demonstrate that the nephrin-induced AKT mediates phosphorylation of several target proteins in podocytes. |
| 170 | 12832477 | One such target is Bad; its phosphorylation and inactivation by 14-3-3 protects podocytes against detachment-induced cell death, suggesting that the nephrin-CD2AP-mediated AKT activity can regulate complex biological programs. |
| 171 | 12832477 | Our findings reveal a novel role for the slit diaphragm proteins nephrin, CD2AP, and podocin and demonstrate that these three proteins, in addition to their structural functions, initiate PI3K/AKT-dependent signal transduction in glomerular podocytes. |
| 172 | 12832477 | Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. |
| 173 | 12832477 | Mutations of NPHS1 or NPHS2, the genes encoding nephrin and podocin, as well as the targeted disruption of CD2-associated protein (CD2AP), lead to heavy proteinuria, suggesting that all three proteins are essential for the integrity of glomerular podocytes, the visceral glomerular epithelial cells of the kidney. |
| 174 | 12832477 | We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate PI3K-dependent AKT signaling in podocytes. |
| 175 | 12832477 | Using two-dimensional gel analysis in combination with a phosphoserine-specific antiserum, we demonstrate that the nephrin-induced AKT mediates phosphorylation of several target proteins in podocytes. |
| 176 | 12832477 | One such target is Bad; its phosphorylation and inactivation by 14-3-3 protects podocytes against detachment-induced cell death, suggesting that the nephrin-CD2AP-mediated AKT activity can regulate complex biological programs. |
| 177 | 12832477 | Our findings reveal a novel role for the slit diaphragm proteins nephrin, CD2AP, and podocin and demonstrate that these three proteins, in addition to their structural functions, initiate PI3K/AKT-dependent signal transduction in glomerular podocytes. |
| 178 | 12832477 | Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. |
| 179 | 12832477 | Mutations of NPHS1 or NPHS2, the genes encoding nephrin and podocin, as well as the targeted disruption of CD2-associated protein (CD2AP), lead to heavy proteinuria, suggesting that all three proteins are essential for the integrity of glomerular podocytes, the visceral glomerular epithelial cells of the kidney. |
| 180 | 12832477 | We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate PI3K-dependent AKT signaling in podocytes. |
| 181 | 12832477 | Using two-dimensional gel analysis in combination with a phosphoserine-specific antiserum, we demonstrate that the nephrin-induced AKT mediates phosphorylation of several target proteins in podocytes. |
| 182 | 12832477 | One such target is Bad; its phosphorylation and inactivation by 14-3-3 protects podocytes against detachment-induced cell death, suggesting that the nephrin-CD2AP-mediated AKT activity can regulate complex biological programs. |
| 183 | 12832477 | Our findings reveal a novel role for the slit diaphragm proteins nephrin, CD2AP, and podocin and demonstrate that these three proteins, in addition to their structural functions, initiate PI3K/AKT-dependent signal transduction in glomerular podocytes. |
| 184 | 12874460 | Protein levels of nephrin, podocin, CD2-associated protein, and podocalyxin were investigated using quantitative immunohistochemical assays. |
| 185 | 12874460 | Real-time PCR was used to determine the mRNA levels of nephrin, podocin, and podoplanin in microdissected glomeruli. |
| 186 | 12874460 | In most acquired renal diseases, except in IgA nephropathy, a marked reduction was observed at the protein levels of nephrin, podocin, and podocalyxin, whereas an increase of the glomerular mRNA levels of nephrin, podocin, and podoplanin was found, compared with controls. |
| 187 | 12874460 | The mean width of the podocyte foot processes was inversely correlated with the protein levels of nephrin (r = -0.443, P < 0.05), whereas it was positively correlated with podoplanin mRNA levels (r = 0.468, P < 0.05) and proteinuria (r = 0.585, P = 0.001). |
| 188 | 12874460 | Protein levels of nephrin, podocin, CD2-associated protein, and podocalyxin were investigated using quantitative immunohistochemical assays. |
| 189 | 12874460 | Real-time PCR was used to determine the mRNA levels of nephrin, podocin, and podoplanin in microdissected glomeruli. |
| 190 | 12874460 | In most acquired renal diseases, except in IgA nephropathy, a marked reduction was observed at the protein levels of nephrin, podocin, and podocalyxin, whereas an increase of the glomerular mRNA levels of nephrin, podocin, and podoplanin was found, compared with controls. |
| 191 | 12874460 | The mean width of the podocyte foot processes was inversely correlated with the protein levels of nephrin (r = -0.443, P < 0.05), whereas it was positively correlated with podoplanin mRNA levels (r = 0.468, P < 0.05) and proteinuria (r = 0.585, P = 0.001). |
| 192 | 12874460 | Protein levels of nephrin, podocin, CD2-associated protein, and podocalyxin were investigated using quantitative immunohistochemical assays. |
| 193 | 12874460 | Real-time PCR was used to determine the mRNA levels of nephrin, podocin, and podoplanin in microdissected glomeruli. |
| 194 | 12874460 | In most acquired renal diseases, except in IgA nephropathy, a marked reduction was observed at the protein levels of nephrin, podocin, and podocalyxin, whereas an increase of the glomerular mRNA levels of nephrin, podocin, and podoplanin was found, compared with controls. |
| 195 | 12874460 | The mean width of the podocyte foot processes was inversely correlated with the protein levels of nephrin (r = -0.443, P < 0.05), whereas it was positively correlated with podoplanin mRNA levels (r = 0.468, P < 0.05) and proteinuria (r = 0.585, P = 0.001). |
| 196 | 12961083 | Expression of nephrin, podocin, alpha-actinin, and WT1 in children with nephrotic syndrome. |
| 197 | 12961083 | Recently, nephrin, podocin, alpha-actinin, and WT1, which are located at the slit diaphragm and expressed by the podocyte, were found to be causative in congenital/familial nephrotic syndrome (NS), but their role in acquired NS remains unclear. |
| 198 | 12961083 | Furthermore, we also found the pattern of distribution of nephrin, podocin, and alpha-actinin changed in children with NS. |
| 199 | 12961083 | In conclusion, a dramatic decrease of podocin expression and abnormal distribution of nephrin, podocin, and alpha-actinin were found in children with NS. |
| 200 | 12961083 | Expression of nephrin, podocin, alpha-actinin, and WT1 in children with nephrotic syndrome. |
| 201 | 12961083 | Recently, nephrin, podocin, alpha-actinin, and WT1, which are located at the slit diaphragm and expressed by the podocyte, were found to be causative in congenital/familial nephrotic syndrome (NS), but their role in acquired NS remains unclear. |
| 202 | 12961083 | Furthermore, we also found the pattern of distribution of nephrin, podocin, and alpha-actinin changed in children with NS. |
| 203 | 12961083 | In conclusion, a dramatic decrease of podocin expression and abnormal distribution of nephrin, podocin, and alpha-actinin were found in children with NS. |
| 204 | 12961083 | Expression of nephrin, podocin, alpha-actinin, and WT1 in children with nephrotic syndrome. |
| 205 | 12961083 | Recently, nephrin, podocin, alpha-actinin, and WT1, which are located at the slit diaphragm and expressed by the podocyte, were found to be causative in congenital/familial nephrotic syndrome (NS), but their role in acquired NS remains unclear. |
| 206 | 12961083 | Furthermore, we also found the pattern of distribution of nephrin, podocin, and alpha-actinin changed in children with NS. |
| 207 | 12961083 | In conclusion, a dramatic decrease of podocin expression and abnormal distribution of nephrin, podocin, and alpha-actinin were found in children with NS. |
| 208 | 12961083 | Expression of nephrin, podocin, alpha-actinin, and WT1 in children with nephrotic syndrome. |
| 209 | 12961083 | Recently, nephrin, podocin, alpha-actinin, and WT1, which are located at the slit diaphragm and expressed by the podocyte, were found to be causative in congenital/familial nephrotic syndrome (NS), but their role in acquired NS remains unclear. |
| 210 | 12961083 | Furthermore, we also found the pattern of distribution of nephrin, podocin, and alpha-actinin changed in children with NS. |
| 211 | 12961083 | In conclusion, a dramatic decrease of podocin expression and abnormal distribution of nephrin, podocin, and alpha-actinin were found in children with NS. |
| 212 | 14523896 | At least three genes have been identified which, when defective, cause familial FSGS or nephrosis: the NPHS1 gene, encoding nephrin; the NPHS2 gene, encoding podocin; and the ACTN4 gene, encoding a-actinin-4. |
| 213 | 14523896 | Because the majority of FSGS cases occur as sporadic disease, the recently described mutations in the NPHS2 gene "in approximately 25 percent of cases of apparently sporadic, steroid-resistant FSGS in children" have claimed great interest. |
| 214 | 14523896 | The applicability of these observations to adults, including the possible importance of the nephrin and alpha-actinin-4 genes in the sporadic disease, remain to be determined. |
| 215 | 14523896 | At least three genes have been identified which, when defective, cause familial FSGS or nephrosis: the NPHS1 gene, encoding nephrin; the NPHS2 gene, encoding podocin; and the ACTN4 gene, encoding a-actinin-4. |
| 216 | 14523896 | Because the majority of FSGS cases occur as sporadic disease, the recently described mutations in the NPHS2 gene "in approximately 25 percent of cases of apparently sporadic, steroid-resistant FSGS in children" have claimed great interest. |
| 217 | 14523896 | The applicability of these observations to adults, including the possible importance of the nephrin and alpha-actinin-4 genes in the sporadic disease, remain to be determined. |
| 218 | 14569107 | For identifying potential diagnostic markers of proteinuric glomerulopathies, glomerular mRNA levels of molecules relevant for podocyte function (alpha-actinin-4, glomerular epithelial protein 1, Wilms tumor antigen 1, synaptopodin, dystroglycan, nephrin, podoplanin, and podocin) were determined by quantitative real-time RT-PCR from microdissected glomeruli. |
| 219 | 14569107 | However, a significant positive correlation between alpha-actinin-4, glomerular epithelial protein 1, synaptopodin, dystroglycan, Wilms tumor antigen 1, and nephrin was found in all analyzed glomeruli, whereas podocin mRNA expression did not correlate. |
| 220 | 14569107 | Expression ratio of podocin to synaptopodin, the two genes with the most disparate expression, allowed a robust separation of FSGS from MCD and nephrosclerosis. |
| 221 | 14569107 | Segregation of FSGS from MCD via this ratio was confirmed in an independent population of formaldehyde-fixed archival biopsies (MCD, n = 5; FSGS, n = 4) after glomerular laser capture microdissection. |
| 222 | 14569107 | In addition, the expression marker was able to predict steroid responsiveness in diagnostically challenging cases of MCD versus FSGS (n = 6). |
| 223 | 14569107 | For identifying potential diagnostic markers of proteinuric glomerulopathies, glomerular mRNA levels of molecules relevant for podocyte function (alpha-actinin-4, glomerular epithelial protein 1, Wilms tumor antigen 1, synaptopodin, dystroglycan, nephrin, podoplanin, and podocin) were determined by quantitative real-time RT-PCR from microdissected glomeruli. |
| 224 | 14569107 | However, a significant positive correlation between alpha-actinin-4, glomerular epithelial protein 1, synaptopodin, dystroglycan, Wilms tumor antigen 1, and nephrin was found in all analyzed glomeruli, whereas podocin mRNA expression did not correlate. |
| 225 | 14569107 | Expression ratio of podocin to synaptopodin, the two genes with the most disparate expression, allowed a robust separation of FSGS from MCD and nephrosclerosis. |
| 226 | 14569107 | Segregation of FSGS from MCD via this ratio was confirmed in an independent population of formaldehyde-fixed archival biopsies (MCD, n = 5; FSGS, n = 4) after glomerular laser capture microdissection. |
| 227 | 14569107 | In addition, the expression marker was able to predict steroid responsiveness in diagnostically challenging cases of MCD versus FSGS (n = 6). |
| 228 | 14569107 | For identifying potential diagnostic markers of proteinuric glomerulopathies, glomerular mRNA levels of molecules relevant for podocyte function (alpha-actinin-4, glomerular epithelial protein 1, Wilms tumor antigen 1, synaptopodin, dystroglycan, nephrin, podoplanin, and podocin) were determined by quantitative real-time RT-PCR from microdissected glomeruli. |
| 229 | 14569107 | However, a significant positive correlation between alpha-actinin-4, glomerular epithelial protein 1, synaptopodin, dystroglycan, Wilms tumor antigen 1, and nephrin was found in all analyzed glomeruli, whereas podocin mRNA expression did not correlate. |
| 230 | 14569107 | Expression ratio of podocin to synaptopodin, the two genes with the most disparate expression, allowed a robust separation of FSGS from MCD and nephrosclerosis. |
| 231 | 14569107 | Segregation of FSGS from MCD via this ratio was confirmed in an independent population of formaldehyde-fixed archival biopsies (MCD, n = 5; FSGS, n = 4) after glomerular laser capture microdissection. |
| 232 | 14569107 | In addition, the expression marker was able to predict steroid responsiveness in diagnostically challenging cases of MCD versus FSGS (n = 6). |
| 233 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 234 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 235 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 236 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 237 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 238 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 239 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 240 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 241 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 242 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 243 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 244 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 245 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 246 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 247 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 248 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 249 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 250 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 251 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 252 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 253 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 254 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 255 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 256 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 257 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 258 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 259 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 260 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 261 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 262 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 263 | 14570703 | Molecular basis of the functional podocin-nephrin complex: mutations in the NPHS2 gene disrupt nephrin targeting to lipid raft microdomains. |
| 264 | 14570703 | Mutations of NPHS1 or NPHS2, the genes encoding for nephrin and podocin, lead to early onset of heavy proteinuria, and rapid progression to end-stage renal disease, suggesting that both proteins are essential for the integrity of the glomerular filter. |
| 265 | 14570703 | Podocin is a stomatin protein family member with a predicted hairpin-like structure localizing to the insertion site of the slit diaphragm of podocytes, the visceral glomerular epithelial cells of the kidney. |
| 266 | 14570703 | The association of podocin with specialized lipid raft microdomains of the plasma membrane was a prerequisite for recruitment of nephrin into rafts. |
| 267 | 14570703 | In contrast, disease-causing mutations of podocin (R138Q and R138X) failed to recruit nephrin into rafts either because these mutants were retained in the endoplasmic reticulum (R138Q), or because they failed to associate with rafts (R138X) despite their presence in the plasma membrane. |
| 268 | 14570703 | Our findings demonstrate that the failure of mutant podocin to recruit nephrin into lipid rafts may be essential for the pathogenesis of NPHS2. |
| 269 | 14638910 | IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was recently reported to have several additional biologic activities. |
| 270 | 14638910 | A receptor for IP-10, CXCR3, showed similar expression patterns to that of IP-10. |
| 271 | 14638910 | The monoclonal anti-IP-10 antibody treatment decreased the expression of IP-10 and podocyte-associated proteins such as nephrin and podocin that are reported to be essential for maintaining the podocyte function (IP-10, 53.0% to control; nephrin, 43.5%; podocin, 60.4%). |
| 272 | 14675423 | Podocin, a plasma membrane anchored stomatin-like protein, is expressed in lipid rafts at the insertion of the slit diaphragm in podocytes. |
| 273 | 14694158 | Podocyte-specific antigens, including WT-1, synaptopodin, nephrin, and podocin, were not expressed by any cells in glomerular crescents, suggesting that podocytes underwent profound phenotypic changes in this nephritis model. |
| 274 | 14712353 | Several molecules, including nephrin, CD2AP, FAT, ZO-1, P-cadherin, Podocin, and Neph 1-3 have all been shown to be associated with the SD complex, and some of these molecules are critical for its integrity. |
| 275 | 15017525 | Discovery of the proteins of the podocyte slit diaphragm, including the nephrin-CD2AP-podocin complex, has represented a major breakthrough in understanding the crucial role of the glomerular epithelial layer in the pathogenesis of proteinuria in human congenital disorders. |
| 276 | 15017525 | The exclusive effect of angiotensin II inhibitors of restoring deficient nephrin expression in proteinuric diseases underlines a close interaction between angiotensin II and podocyte proteins and indicates a fresh way to look at the renoprotective properties of these molecules. |
| 277 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 278 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 279 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 280 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 281 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 282 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 283 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 284 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 285 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 286 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 287 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 288 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 289 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 290 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 291 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 292 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 293 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 294 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 295 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 296 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 297 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 298 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 299 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 300 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 301 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 302 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 303 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 304 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 305 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 306 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 307 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 308 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 309 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 310 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 311 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 312 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 313 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 314 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 315 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 316 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 317 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 318 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 319 | 15363039 | Nephrin, podocin and alpha-actinin are all involved in proteinuria, but it is unclear which molecular event plays a crucial role during the development of proteinuria. |
| 320 | 15363039 | Two days after PAN injection, nephrin and podocin staining became discontinuous, podocin intensity decreased and FP swelled. |
| 321 | 15363039 | Both podocin and nephrin intensity decreased dramatically when heavy proteinuria occurred, but nephrin mRNA was regained. |
| 322 | 15363039 | When proteinuria disappeared, podocin recovered whereas nephrin did not (P = 0.02); alpha-actinin intensity increased (P = 0.009) and the distribution changed. |
| 323 | 15363039 | The podocyte FP volume density correlated negatively with nephrin (r = -0.78, P = 0.0001) and podocin immunofluorescence intensity (r = -0.76, P = 0.0001). |
| 324 | 15363039 | We conclude that, before the onset of proteinuria, the first response was the nephrin and podocin distribution change, podocin protein decrease and swollen FP; the podocin quantitative change was earlier than nephrin. |
| 325 | 15363039 | Podocin and nephrin distribution and the protein level was associated with proteinuria more closely than their mRNA level. |
| 326 | 15367484 | Congenital nephrotic syndrome (CNS) is clinically and genetically heterogeneous, with mutations in WT1, NPHS1 and NPHS2 accounting for part of cases. |
| 327 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 328 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 329 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 330 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 331 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 332 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 333 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 334 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 335 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 336 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 337 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 338 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 339 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 340 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 341 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 342 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 343 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 344 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 345 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 346 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 347 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 348 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 349 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 350 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 351 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 352 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 353 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 354 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 355 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 356 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 357 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 358 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 359 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 360 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 361 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 362 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 363 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 364 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 365 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 366 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 367 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 368 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 369 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 370 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 371 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 372 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 373 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 374 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 375 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 376 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 377 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 378 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 379 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 380 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 381 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 382 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 383 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 384 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 385 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 386 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 387 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 388 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 389 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 390 | 15388893 | Effect of the knockdown of podocin mRNA on nephrin and alpha-actinin in mouse podocyte. |
| 391 | 15388893 | Recently, the novel podocyte proteins podocin, nephrin, and alpha-actinin-4 have been identified in three congenital/family nephrotic syndromes, respectively. |
| 392 | 15388893 | In this study, to investigate the molecular interactions among podocin, nephrin, and alpha-actinin-4, we reconstructed the RNA interference (RNAi) expression vector, pSilencer 2.1-U6, specifically targeting podocin mRNA, and it was transfected into the mouse podocyte clone (MPC5). |
| 393 | 15388893 | Immunofluorescence staining, double-immunolabeling, confocal microscopy, semiquantitative reverse transcription polymerase chain reaction (RT-PCR), and Western blotting were used to detect the distribution and expression of podocin, nephrin, alpha-actinin-4, and glyseraldehyde-3-phosphate dehydrogenase (GAPDH)/beta-actin. |
| 394 | 15388893 | The fluorescence intensity of podocin and nephrin decreased obviously, along with the evident distribution change from the cell membrane surface to the nucleus circumference in podocyte. |
| 395 | 15388893 | In relation to GAPDH, the mRNA reductions of podocin and nephrin were observed by about 65% and 70%, respectively. |
| 396 | 15388893 | In relation to beta-actin, the protein level of nephrin decreased by about 78%. |
| 397 | 15388893 | Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change. |
| 398 | 15388893 | These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin. |
| 399 | 15465010 | In contrast, podocin and CD2AP, two proteins shown to interact with nephrin in the slit diaphragm, are acutely downregulated at days 3-7 and, thereafter, recovered again to normal levels after 29 days. |
| 400 | 15465010 | In summary, our data show that in the course of mesangioproliferative glomerulonephritis in rats, an upregulation of nephrin expression occurs with a concomitant transient downregulation of podocin and CD2AP which may account for a highly dysregulated filtration barrier and increased proteinuria. |
| 401 | 15465010 | In contrast, podocin and CD2AP, two proteins shown to interact with nephrin in the slit diaphragm, are acutely downregulated at days 3-7 and, thereafter, recovered again to normal levels after 29 days. |
| 402 | 15465010 | In summary, our data show that in the course of mesangioproliferative glomerulonephritis in rats, an upregulation of nephrin expression occurs with a concomitant transient downregulation of podocin and CD2AP which may account for a highly dysregulated filtration barrier and increased proteinuria. |
| 403 | 15500127 | Recently slit membrane-associated molecules (CD2AP, alpha-actinin 4 and podocin) and angiotensin II type I receptor in the podocyte have been clearly shown to be relevant for the pathogenesis of FSGS. |
| 404 | 15505531 | The glomerular basement membrane is composed of a multitude of proteins, including collagen IV, heparan sulfate proteoglycans, and laminin, among others. |
| 405 | 15505531 | The exact mechanism by which nephrin controls permselectivity is not yet clear, but it is known to interact with several podocyte proteins including CD2AP, podocin, and alpha-actinin-4. |
| 406 | 15505531 | A host of transcription factors, especially WT1 and PAX2, play a significant role in modulating podocyte function. |
| 407 | 15579500 | The electrophysiologic properties of a conditionally immortalized human podocyte cell line that expresses the specific podocyte proteins nephrin, podocin, and synaptopodin were examined by patch clamp. |
| 408 | 15616033 | TERalb (%/h) was similar in normoalbuminuric and microalbuminuric group 1, 2, and 3 diabetic patients (medians: 14.1 vs. 14.4 vs. 15.7 vs. 14.9, respectively) (ANOVA, NS). mRNA expression of slit diaphragm proteins CD2AP, FAT, Actn 4, NPHS1, and NPHS2 was higher in normoalbuminuric patients than in microalbuminuric patients (groups 1, 2, and 3) (ANOVA, P < 0.001). |
| 409 | 15634346 | CD2AP, podocin, Fyn kinase, and phosphoinositide 3-kinase are reported intracellular interacting partners of nephrin, although the biological roles of these interactions are unclarified. |
| 410 | 15634346 | Peptide mass fingerprinting and amino acid sequencing identified this protein as IQGAP1, an effector protein of small GTPases Rac1 and Cdc42 and a putative regulator of cell-cell adherens junctions. |
| 411 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 412 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 413 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 414 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 415 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 416 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 417 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 418 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 419 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 420 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 421 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 422 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 423 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 424 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 425 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 426 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 427 | 15780077 | Analysis of NPHS1, NPHS2, ACTN4, and WT1 in Japanese patients with congenital nephrotic syndrome. |
| 428 | 15843471 | During the calcium switch, there were reversible changes in localization and detergent solubility of the slit diaphragm protein ZO-1 and alpha-actinin-4, whereas nephrin and podocin solubility were unchanged. |
| 429 | 15843475 | NEPH2 is located at the glomerular slit diaphragm, interacts with nephrin and is cleaved from podocytes by metalloproteinases. |
| 430 | 15843475 | The NEPH family comprises three transmembrane proteins of the Ig superfamily interacting with the glomerular slit diaphragm proteins podocin and ZO-1. |
| 431 | 15843475 | The authors localized the expression of NEPH2 to the glomerular slit diaphragm by electron microscopy and show NEPH2 homodimerization and specific interactions with the extracellular domain of nephrin in vitro and in vivo. |
| 432 | 15843475 | The results suggest a role for NEPH2 in the organization and/or maintenance of the glomerular slit diaphragm that may differ from the functions of NEPH1 and nephrin. |
| 433 | 15882266 | Nephrin and podocin dissociate at the onset of proteinuria in experimental membranous nephropathy. |
| 434 | 15888021 | Recent findings on podocin genomics, the permeability factor and CD80 expression may ultimately lead to a better understanding of recurrent FSGS as well as a more effective approach to its prevention and treatment. |
| 435 | 15942677 | Direct effect of plasma permeability factors from patients with idiopatic FSGS on nephrin and podocin expression in human podocytes. |
| 436 | 15942677 | Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes. |
| 437 | 15942677 | Nephrin and podocin expression was semi-quantitatively evaluated by immunofluorescence. |
| 438 | 15942677 | We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes. |
| 439 | 15942677 | On the contrary, podocin expression was unchanged after incubation with serum and PF from FSGS patients for short periods, but markedly reduced at 24 h. |
| 440 | 15942677 | Our results demonstrate that serum and PF from FSGS patients may directly affect nephrin and podocin in human podocytes, thus providing new insights into the mechanisms causing proteinuria in FSGS. |
| 441 | 15942677 | Direct effect of plasma permeability factors from patients with idiopatic FSGS on nephrin and podocin expression in human podocytes. |
| 442 | 15942677 | Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes. |
| 443 | 15942677 | Nephrin and podocin expression was semi-quantitatively evaluated by immunofluorescence. |
| 444 | 15942677 | We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes. |
| 445 | 15942677 | On the contrary, podocin expression was unchanged after incubation with serum and PF from FSGS patients for short periods, but markedly reduced at 24 h. |
| 446 | 15942677 | Our results demonstrate that serum and PF from FSGS patients may directly affect nephrin and podocin in human podocytes, thus providing new insights into the mechanisms causing proteinuria in FSGS. |
| 447 | 15942677 | Direct effect of plasma permeability factors from patients with idiopatic FSGS on nephrin and podocin expression in human podocytes. |
| 448 | 15942677 | Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes. |
| 449 | 15942677 | Nephrin and podocin expression was semi-quantitatively evaluated by immunofluorescence. |
| 450 | 15942677 | We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes. |
| 451 | 15942677 | On the contrary, podocin expression was unchanged after incubation with serum and PF from FSGS patients for short periods, but markedly reduced at 24 h. |
| 452 | 15942677 | Our results demonstrate that serum and PF from FSGS patients may directly affect nephrin and podocin in human podocytes, thus providing new insights into the mechanisms causing proteinuria in FSGS. |
| 453 | 15942677 | Direct effect of plasma permeability factors from patients with idiopatic FSGS on nephrin and podocin expression in human podocytes. |
| 454 | 15942677 | Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes. |
| 455 | 15942677 | Nephrin and podocin expression was semi-quantitatively evaluated by immunofluorescence. |
| 456 | 15942677 | We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes. |
| 457 | 15942677 | On the contrary, podocin expression was unchanged after incubation with serum and PF from FSGS patients for short periods, but markedly reduced at 24 h. |
| 458 | 15942677 | Our results demonstrate that serum and PF from FSGS patients may directly affect nephrin and podocin in human podocytes, thus providing new insights into the mechanisms causing proteinuria in FSGS. |
| 459 | 15942677 | Direct effect of plasma permeability factors from patients with idiopatic FSGS on nephrin and podocin expression in human podocytes. |
| 460 | 15942677 | Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes. |
| 461 | 15942677 | Nephrin and podocin expression was semi-quantitatively evaluated by immunofluorescence. |
| 462 | 15942677 | We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes. |
| 463 | 15942677 | On the contrary, podocin expression was unchanged after incubation with serum and PF from FSGS patients for short periods, but markedly reduced at 24 h. |
| 464 | 15942677 | Our results demonstrate that serum and PF from FSGS patients may directly affect nephrin and podocin in human podocytes, thus providing new insights into the mechanisms causing proteinuria in FSGS. |
| 465 | 15954902 | ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo. |
| 466 | 15968559 | Also, the genes encoding the four major slit diaphragm proteins, nephrin, podocin, Neph1 and CD2-associated protein were sequenced in 38 patients with MCNS of varying severity. |
| 467 | 15968559 | The genetic analyses revealed heterozygous amino acid changes in nephrin and podocin in 10 of the 38 patients studied. |
| 468 | 15968559 | On the other hand, the genes coding for Neph1 and CD2AP were highly conserved and no amino acid substitutions were detected. |
| 469 | 15968559 | Also, the genes encoding the four major slit diaphragm proteins, nephrin, podocin, Neph1 and CD2-associated protein were sequenced in 38 patients with MCNS of varying severity. |
| 470 | 15968559 | The genetic analyses revealed heterozygous amino acid changes in nephrin and podocin in 10 of the 38 patients studied. |
| 471 | 15968559 | On the other hand, the genes coding for Neph1 and CD2AP were highly conserved and no amino acid substitutions were detected. |
| 472 | 15997642 | The main components of the slit diaphragm are nephrin, the product of NPHS1 gene and podocin, the product of NPHS2 gene. |
| 473 | 15997642 | Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS). |
| 474 | 15997642 | Reduced expression and redistribution of nephrin and podocin are also seen in podocytes of patients with acquired glomerulopathies. |
| 475 | 15997642 | Together with podocin and CD2AP (CD2-associated protein), nephrin forms a complex determining the integrity of the slit diaphragm. |
| 476 | 15997642 | The main components of the slit diaphragm are nephrin, the product of NPHS1 gene and podocin, the product of NPHS2 gene. |
| 477 | 15997642 | Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS). |
| 478 | 15997642 | Reduced expression and redistribution of nephrin and podocin are also seen in podocytes of patients with acquired glomerulopathies. |
| 479 | 15997642 | Together with podocin and CD2AP (CD2-associated protein), nephrin forms a complex determining the integrity of the slit diaphragm. |
| 480 | 15997642 | The main components of the slit diaphragm are nephrin, the product of NPHS1 gene and podocin, the product of NPHS2 gene. |
| 481 | 15997642 | Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS). |
| 482 | 15997642 | Reduced expression and redistribution of nephrin and podocin are also seen in podocytes of patients with acquired glomerulopathies. |
| 483 | 15997642 | Together with podocin and CD2AP (CD2-associated protein), nephrin forms a complex determining the integrity of the slit diaphragm. |
| 484 | 15997642 | The main components of the slit diaphragm are nephrin, the product of NPHS1 gene and podocin, the product of NPHS2 gene. |
| 485 | 15997642 | Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS). |
| 486 | 15997642 | Reduced expression and redistribution of nephrin and podocin are also seen in podocytes of patients with acquired glomerulopathies. |
| 487 | 15997642 | Together with podocin and CD2AP (CD2-associated protein), nephrin forms a complex determining the integrity of the slit diaphragm. |
| 488 | 16102746 | Organization of the pronephric filtration apparatus in zebrafish requires Nephrin, Podocin and the FERM domain protein Mosaic eyes. |
| 489 | 16102746 | We first characterized the function of the zebrafish homolog of Nephrin, the disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome. |
| 490 | 16102746 | Zebrafish nephrin and podocin were specifically expressed in pronephric podocytes and required for the development of pronephric podocyte cell structure. |
| 491 | 16102746 | Ultrastructurally, disruption of nephrin or podocin expression resulted in a loss of slit-diaphragms at 72 and 96 h post-fertilization and failure to form normal podocyte foot processes. |
| 492 | 16102746 | A functional assay of glomerular filtration barrier revealed that absence of normal nephrin, podocin or mosaic eyes expression results in loss of glomerular filtration discrimination and aberrant passage of high molecular weight substances into the glomerular filtrate. |
| 493 | 16102746 | Organization of the pronephric filtration apparatus in zebrafish requires Nephrin, Podocin and the FERM domain protein Mosaic eyes. |
| 494 | 16102746 | We first characterized the function of the zebrafish homolog of Nephrin, the disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome. |
| 495 | 16102746 | Zebrafish nephrin and podocin were specifically expressed in pronephric podocytes and required for the development of pronephric podocyte cell structure. |
| 496 | 16102746 | Ultrastructurally, disruption of nephrin or podocin expression resulted in a loss of slit-diaphragms at 72 and 96 h post-fertilization and failure to form normal podocyte foot processes. |
| 497 | 16102746 | A functional assay of glomerular filtration barrier revealed that absence of normal nephrin, podocin or mosaic eyes expression results in loss of glomerular filtration discrimination and aberrant passage of high molecular weight substances into the glomerular filtrate. |
| 498 | 16102746 | Organization of the pronephric filtration apparatus in zebrafish requires Nephrin, Podocin and the FERM domain protein Mosaic eyes. |
| 499 | 16102746 | We first characterized the function of the zebrafish homolog of Nephrin, the disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome. |
| 500 | 16102746 | Zebrafish nephrin and podocin were specifically expressed in pronephric podocytes and required for the development of pronephric podocyte cell structure. |
| 501 | 16102746 | Ultrastructurally, disruption of nephrin or podocin expression resulted in a loss of slit-diaphragms at 72 and 96 h post-fertilization and failure to form normal podocyte foot processes. |
| 502 | 16102746 | A functional assay of glomerular filtration barrier revealed that absence of normal nephrin, podocin or mosaic eyes expression results in loss of glomerular filtration discrimination and aberrant passage of high molecular weight substances into the glomerular filtrate. |
| 503 | 16102746 | Organization of the pronephric filtration apparatus in zebrafish requires Nephrin, Podocin and the FERM domain protein Mosaic eyes. |
| 504 | 16102746 | We first characterized the function of the zebrafish homolog of Nephrin, the disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome. |
| 505 | 16102746 | Zebrafish nephrin and podocin were specifically expressed in pronephric podocytes and required for the development of pronephric podocyte cell structure. |
| 506 | 16102746 | Ultrastructurally, disruption of nephrin or podocin expression resulted in a loss of slit-diaphragms at 72 and 96 h post-fertilization and failure to form normal podocyte foot processes. |
| 507 | 16102746 | A functional assay of glomerular filtration barrier revealed that absence of normal nephrin, podocin or mosaic eyes expression results in loss of glomerular filtration discrimination and aberrant passage of high molecular weight substances into the glomerular filtrate. |
| 508 | 16102746 | Organization of the pronephric filtration apparatus in zebrafish requires Nephrin, Podocin and the FERM domain protein Mosaic eyes. |
| 509 | 16102746 | We first characterized the function of the zebrafish homolog of Nephrin, the disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the gene mutated in autosomal recessive steroid-resistant nephrotic syndrome. |
| 510 | 16102746 | Zebrafish nephrin and podocin were specifically expressed in pronephric podocytes and required for the development of pronephric podocyte cell structure. |
| 511 | 16102746 | Ultrastructurally, disruption of nephrin or podocin expression resulted in a loss of slit-diaphragms at 72 and 96 h post-fertilization and failure to form normal podocyte foot processes. |
| 512 | 16102746 | A functional assay of glomerular filtration barrier revealed that absence of normal nephrin, podocin or mosaic eyes expression results in loss of glomerular filtration discrimination and aberrant passage of high molecular weight substances into the glomerular filtrate. |
| 513 | 16186681 | Associations with various genes (NPHS1, ACTN4, NPHS2, WT-1) and linkage to several chromosomal regions (such as 19q13, 11q21, 11q24) have been reported in patients with familial NS/FSGS. |
| 514 | 16382022 | IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was reported recently to have several additional biologic activities. |
| 515 | 16382022 | In cultured podocytes subjected to recombinant IP-10 treatment, the expression of slit-diaphragm (SD) components nephrin and podocin clearly was heightened. |
| 516 | 16382022 | Rats that had puromycin aminonucleoside nephropathy and anti-nephrin antibody-induced nephropathy and were subjected to anti-IP-10 function-blocking antibody (anti-IP-10 mAb) treatment displayed a decrease in the protein level of SD components, as well as exacerbated proteinuria. |
| 517 | 16382022 | Cultured podocytes subjected to recombinant IP-10 treatment displayed an increase in the protein level of p27(Kip1), whereas the levels of cyclins E and A decreased. |
| 518 | 16382022 | The expression of IP-10 and SD components was heightened by the treatment of siRNA of cyclin A, whereas these expressions were lowered by the treatment of siRNA of p27(Kip1). |
| 519 | 16382022 | Proteinuric rats subjected to anti-IP-10 mAb treatment displayed a heightened expression of cyclin A from the early phase of the disease, which indicates that the anti-IP-10 mAb treatment exacerbates podocyte injury by disturbing the cell-cycle balance. |
| 520 | 16452496 | Immunofluorescence studies of podocyte-associated proteins nephrin and podocin revealed diminished and discontinuous staining patterns in rats with PAN nephrosis, indicating severe podocyte injury. |
| 521 | 16452496 | Fluvastatin also mitigated tubulointerstitial damage in PAN nephrosis, with the repression of PAN-induced NF-kappaB and activator protein-1 activation in the kidneys. |
| 522 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 523 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 524 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 525 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 526 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 527 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 528 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 529 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 530 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 531 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 532 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 533 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 534 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 535 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 536 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 537 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 538 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 539 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 540 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 541 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 542 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 543 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 544 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 545 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 546 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 547 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 548 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 549 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 550 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 551 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 552 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 553 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 554 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 555 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 556 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 557 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 558 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 559 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 560 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 561 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 562 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 563 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 564 | 16501493 | The relationship among nephrin, podocin, CD2AP, and alpha-actinin might not be a true 'interaction' in podocyte. |
| 565 | 16501493 | The abnormality of a single podocyte molecule, caused by a single gene mutation, such as NPHS1, NPHS2, CD2AP, and ACTN4, can lead to the hereditary/congenital nephrotic syndromes (NS). |
| 566 | 16501493 | We respectively knockdown the nephrin, podocin, CD2AP, or alpha-actinin-4 mRNA by using reconstructed RNA interference vector--psiRNA-hH1GFPzeo in mouse podocyte clone. |
| 567 | 16501493 | With nephrin knockdown, only CD2AP increased, whereas podocin showed no change. |
| 568 | 16501493 | Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased. |
| 569 | 16501493 | Nephrin, podocin, or CD2AP knockdown did not change the expression of alpha-actinin-4, whereas alpha-actinin-4 knockdown begetted the reduction of nephrin, and the increment of podocin and CD2AP. |
| 570 | 16501493 | The redistributions of nephrin, podocin, and CD2AP were revealed around a predominant nuclear staining compared with the membrane surface staining in the control podocytes. |
| 571 | 16533308 | On the cellular level--using immunostaining--we detected cells expressing podocin, nephrin and wt-1, characteristic for differentiated podocytes and other cells, which expressed Tamm-Horsfall protein, a marker for distal tubule epithelial cells of kidney tissue. |
| 572 | 16541019 | Sema 3A decreased semaphorin 3B, plexin A1, A3, and D1 >/=50% and reduced plexin A2 mRNA to undetectable levels. |
| 573 | 16541019 | Sema 3A induced a dose-response podocin downregulation and decreased its interaction with CD2-associated protein and nephrin, as determined by Western analysis and co-immunoprecipitation. |
| 574 | 16541019 | Sema 3A induced a 10-fold increase in podocyte apoptosis and significantly decreased the activity of the Akt survival pathway. |
| 575 | 16597608 | Autocrine VEGF-A system in podocytes regulates podocin and its interaction with CD2AP. |
| 576 | 16597608 | Here, we examined the expression of VEGF-A and its receptors VEGFR1, VEGFR2, NP1, and NP2 in conditionally immortalized mouse podocytes cultured in undifferentiated and differentiated conditions using RT-PCR and Western analysis. |
| 577 | 16597608 | Differentiated podocytes expressed eightfold higher VEGFR2 mRNA levels than undifferentiated podocytes, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels were similar. |
| 578 | 16597608 | VEGF(165) induced a twofold increase in VEGFR2 mRNA and protein levels, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels remained unchanged. |
| 579 | 16597608 | VEGF(165) induced VEGFR2 phosphorylation. |
| 580 | 16597608 | We determined that VEGF-A signaling regulates slit diaphragm proteins by inducing a dose-response podocin upregulation and increasing its interaction with CD2AP. |
| 581 | 16597608 | VEGF-A functions in podocytes include promoting survival through VEGFR2, inducing podocin upregulation and increasing podocin/CD2AP interaction. |
| 582 | 16597608 | Autocrine VEGF-A system in podocytes regulates podocin and its interaction with CD2AP. |
| 583 | 16597608 | Here, we examined the expression of VEGF-A and its receptors VEGFR1, VEGFR2, NP1, and NP2 in conditionally immortalized mouse podocytes cultured in undifferentiated and differentiated conditions using RT-PCR and Western analysis. |
| 584 | 16597608 | Differentiated podocytes expressed eightfold higher VEGFR2 mRNA levels than undifferentiated podocytes, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels were similar. |
| 585 | 16597608 | VEGF(165) induced a twofold increase in VEGFR2 mRNA and protein levels, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels remained unchanged. |
| 586 | 16597608 | VEGF(165) induced VEGFR2 phosphorylation. |
| 587 | 16597608 | We determined that VEGF-A signaling regulates slit diaphragm proteins by inducing a dose-response podocin upregulation and increasing its interaction with CD2AP. |
| 588 | 16597608 | VEGF-A functions in podocytes include promoting survival through VEGFR2, inducing podocin upregulation and increasing podocin/CD2AP interaction. |
| 589 | 16597608 | Autocrine VEGF-A system in podocytes regulates podocin and its interaction with CD2AP. |
| 590 | 16597608 | Here, we examined the expression of VEGF-A and its receptors VEGFR1, VEGFR2, NP1, and NP2 in conditionally immortalized mouse podocytes cultured in undifferentiated and differentiated conditions using RT-PCR and Western analysis. |
| 591 | 16597608 | Differentiated podocytes expressed eightfold higher VEGFR2 mRNA levels than undifferentiated podocytes, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels were similar. |
| 592 | 16597608 | VEGF(165) induced a twofold increase in VEGFR2 mRNA and protein levels, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels remained unchanged. |
| 593 | 16597608 | VEGF(165) induced VEGFR2 phosphorylation. |
| 594 | 16597608 | We determined that VEGF-A signaling regulates slit diaphragm proteins by inducing a dose-response podocin upregulation and increasing its interaction with CD2AP. |
| 595 | 16597608 | VEGF-A functions in podocytes include promoting survival through VEGFR2, inducing podocin upregulation and increasing podocin/CD2AP interaction. |
| 596 | 16611717 | No significant reduction of slit membrane molecules (podocin and nephrin), key GBM components (fibronectin, laminins, and collagen IV isoforms), or podocyte integrins could be observed at onset of proteinuria. |
| 597 | 16628251 | Defects in several podocyte proteins have been implicated in the etiology of FSGS, including podocin, alpha-actinin-4, CD2-associated protein (CD2AP), and TRPC6. |
| 598 | 16628251 | Combinations of Cd2ap heterozygosity and heterozygosity of either synaptopodin (Synpo) or Fyn proto-oncogene (Fyn) but not kin of IRRE like 1 (Neph1) resulted in spontaneous proteinuria and in FSGS-like glomerular damage. |
| 599 | 16628251 | These genetic interactions were also reflected at a functional level, as we found that CD2AP associates with Fyn and Synpo but not with Neph1. |
| 600 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 601 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 602 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 603 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 604 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 605 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 606 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 607 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 608 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 609 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 610 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 611 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 612 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 613 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 614 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 615 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 616 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 617 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 618 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 619 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 620 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 621 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 622 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 623 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 624 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 625 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 626 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 627 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 628 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 629 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 630 | 16636307 | Nephrin, podocin, CD2AP, and alpha-actinin-4 are important podocyte proteins that help maintain the integrity of the slit diaphragm and prevent proteinuria. |
| 631 | 16636307 | In this study, changes in the expression and distribution of nephrin, podocin, CD2AP, and alpha-actinin-4 were dynamically detected in Adriamycin-induced nephrotic (ADR) rats treated with three different drugs: lisinopril, prednisone, and ATRA. |
| 632 | 16636307 | The distribution and the expression of messenger RNA and protein of nephrin, podocin, CD2AP, and alpha-actinin-4 were detected by indirect immunofluorescence, real-time polymerase chain reaction, and Western blotting, respectively. |
| 633 | 16636307 | With the intervention of lisinopril, prednisone, and ATRA, changes in the expression of nephrin, podocin, and CD2AP were diverse, which was different from that detected in ADR rats. |
| 634 | 16636307 | After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention. |
| 635 | 16636307 | In summary, we conclude that the antiproteinuric effects of lisinopril, prednisone, and ATRA were achieved by changes in the expression and distribution of the important podocyte molecules nephrin, podocin, CD2AP, and alpha-actinin-4. |
| 636 | 16703378 | Angiotensin converting enzyme (ACE) and prostaglandin synthesis inhibition along with supportive albumin infusion therapy, with or without unilateral nephrectomy, has allowed management of the disease without dialysis until transplantation in some cases of congenital nephrotic syndrome. |
| 637 | 16703378 | Reported here is a case of heterozygous NPHS1 mutation, with normal NPHS2 gene structure, presenting during prenatal screening and developing nephrotic syndrome within days of birth. |
| 638 | 16710349 | No change from base line values was observed as for hs-C-reactive protein and interleukin-6. |
| 639 | 16710349 | Real-time polymerase chain reaction measurement of mRNA SD proteins (CD2AP, FAT, Actn 4, NPHS1, and NPHS2) significantly increased in kidney biopsy specimens after simvastatin, but not cholestyramine treatment. |
| 640 | 16752799 | Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2. |
| 641 | 16752799 | Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes. |
| 642 | 16752799 | It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2). |
| 643 | 16752799 | This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele. |
| 644 | 16752799 | There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models). |
| 645 | 16752799 | Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2. |
| 646 | 16752799 | Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes. |
| 647 | 16752799 | It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2). |
| 648 | 16752799 | This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele. |
| 649 | 16752799 | There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models). |
| 650 | 16752799 | Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2. |
| 651 | 16752799 | Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes. |
| 652 | 16752799 | It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2). |
| 653 | 16752799 | This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele. |
| 654 | 16752799 | There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models). |
| 655 | 16752799 | Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2. |
| 656 | 16752799 | Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes. |
| 657 | 16752799 | It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2). |
| 658 | 16752799 | This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele. |
| 659 | 16752799 | There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models). |
| 660 | 16837631 | ILK deficiency caused an aberrant distribution of nephrin and alpha-actinin-4 in podocytes, whereas the localization of podocin and synaptopodin remained relatively intact. |
| 661 | 16837631 | Co-immunoprecipitation demonstrated that ILK physically interacted with nephrin to form a ternary complex, and alpha-actinin-4 participated in ILK/nephrin complex formation. |
| 662 | 16837631 | Therefore, ILK plays an essential role in specifying nephrin and alpha-actinin-4 distribution and in maintaining the slit diaphragm integrity and podocyte architecture. |
| 663 | 16841182 | Podocyte-associated proteins FAT, alpha-actinin-4 and filtrin are expressed in Langerhans islets of the pancreas. |
| 664 | 16841182 | Recently, genetic mapping of proteinuric kidney disease genes and animal models have revealed further important molecules for the kidney filtration function including alpha-actinin-4, podocin, FAT, and NEPH1. |
| 665 | 16841182 | This study was addressed to explore the pancreatic expression of the podocyte molecules podocin, FAT, alpha-actinin-4, NEPH1, NEPH2, filtrin/NEPH3, synaptopodin and CD2 associated protein (CD2AP). |
| 666 | 16841182 | Of the nephrin-associated podocyte proteins, filtrin/NEPH3, FAT, and alpha-actinin-4 were found to be expressed in the pancreas at the gene and protein level and localized to Langerhans islets. |
| 667 | 16841182 | Podocyte-associated proteins FAT, alpha-actinin-4 and filtrin are expressed in Langerhans islets of the pancreas. |
| 668 | 16841182 | Recently, genetic mapping of proteinuric kidney disease genes and animal models have revealed further important molecules for the kidney filtration function including alpha-actinin-4, podocin, FAT, and NEPH1. |
| 669 | 16841182 | This study was addressed to explore the pancreatic expression of the podocyte molecules podocin, FAT, alpha-actinin-4, NEPH1, NEPH2, filtrin/NEPH3, synaptopodin and CD2 associated protein (CD2AP). |
| 670 | 16841182 | Of the nephrin-associated podocyte proteins, filtrin/NEPH3, FAT, and alpha-actinin-4 were found to be expressed in the pancreas at the gene and protein level and localized to Langerhans islets. |
| 671 | 16889564 | Nephrin and podocin were identified as gene products mutated in Finnish-type congenital nephrotic syndrome and autosomal recessive steroid-resistant nephrotic syndrome, respectively. |
| 672 | 16889564 | The expression of nephrin and podocin was reduced in glomeruli of minimal change nephrotic syndrome, which suggested that the altered expression of these molecules contributes to the development of proteinuria also in acquired diseases. |
| 673 | 16889564 | Some recent studies demonstrated that CD2-associated protein (CD2AP) is also a functional molecule in the slit diaphragm, and its expression is altered in membranous nephropathy. |
| 674 | 16889564 | Nephrin and podocin were identified as gene products mutated in Finnish-type congenital nephrotic syndrome and autosomal recessive steroid-resistant nephrotic syndrome, respectively. |
| 675 | 16889564 | The expression of nephrin and podocin was reduced in glomeruli of minimal change nephrotic syndrome, which suggested that the altered expression of these molecules contributes to the development of proteinuria also in acquired diseases. |
| 676 | 16889564 | Some recent studies demonstrated that CD2-associated protein (CD2AP) is also a functional molecule in the slit diaphragm, and its expression is altered in membranous nephropathy. |
| 677 | 16898497 | Gene mutations for nephrin, podocin, WT1, alpha-actinin 4 cause the damage of filtration barrier of glomerulus and proteinuria in consequence. |
| 678 | 16932440 | Nephrin, Neph1 and podocin seem to form a multifunctional receptor complex at the slit diaphragm. |
| 679 | 16943305 | The expression of podocyte-specific proteins (podocalyxin, glomerular epithelial protein-1, podocin, nephrin, synaptopodin, and alpha-actinin-4), podocyte synthesized proteins (vascular endothelial growth factor and novH), transcription factors (WT1 and PAX2), cyclin-dependent kinase inhibitor p57, and intermediate filaments (cytokeratins and vimentin) was tested. |
| 680 | 16943305 | WT1 and p57 were expressed in some parietal cells, whereas PAX2 was present in all or most of them, so some parietal cells coexpressed WT1 and PAX2. |
| 681 | 16968782 | The Src-family member Yes, known to enhance podocin-nephrin interaction by nephrin phosphorylation, diminishes beta-arrestin2-nephrin interaction. beta-Arrestin2 induces nephrin endocytosis and attenuates nephrin signaling. |
| 682 | 17182884 | Treatment with atRA reduced cell proliferation rate by causing G1 arrest and restored the expression of the differentiation markers (synaptopodin, nephrin, podocin, and WT-1) in HIV-1-infected podocytes. |
| 683 | 17182884 | Podocytes expressed most isoforms of retinoic acid receptors (RAR) and retinoid X receptors (RXR) with the exception of RXRgamma. |
| 684 | 17182884 | Furthermore, both atRA and forskolin suppressed HIV-induced mitogen-activated protein kinase 1 and 2 and Stat3 phosphorylation. |
| 685 | 17200434 | Notably, gene expressions of podocyte-associated molecules nephrin and podocin were markedly decreased in aldosterone-infused rats at 2 weeks, with a gradual decrease thereafter. |
| 686 | 17200434 | Podocyte injury was accompanied by renal reduced nicotinamide-adenine dinucleotide phosphate oxidase activation, increased oxidative stress, and enhanced expression of aldosterone effector kinase Sgk1. |
| 687 | 17200434 | In addition, proteinuria, podocyte damage, and Sgk1 upregulation were significantly alleviated by tempol, a membrane-permeable superoxide dismutase, suggesting the pathogenic role of oxidative stress. |
| 688 | 17200434 | In cultured podocytes with consistent expression of mineralocorticoid receptor, aldosterone stimulated membrane translocation of reduced nicotinamide-adenine dinucleotide phosphate oxidase cytosolic components and oxidative stress generation in podocytes. |
| 689 | 17200434 | Furthermore, aldosterone enhanced the expression of Sgk1, which was inhibited by mineralocorticoid receptor antagonist and tempol. |
| 690 | 17211152 | NPHS1 and NPHS2 gene mutations in Chinese children with sporadic nephrotic syndrome. |
| 691 | 17211152 | Mutational analyses of NPHS1 and NPHS2 were performed to verify this hypothesis in sporadic nephrotic syndrome (NS) patients. |
| 692 | 17211152 | Direct sequencing was performed after PCR amplification of all 29 and 8 exons of the NPHS1 and NPHS2 genes, respectively. |
| 693 | 17211152 | The results demonstrate that NPHS1 and NPHS2 mutations are also present in Chinese sporadic NS patients, suggesting that genetic changes of nephrin and podocin may play pathogenetic roles in some patients with sporadic steroid resistant NS. |
| 694 | 17211152 | NPHS1 and NPHS2 gene mutations in Chinese children with sporadic nephrotic syndrome. |
| 695 | 17211152 | Mutational analyses of NPHS1 and NPHS2 were performed to verify this hypothesis in sporadic nephrotic syndrome (NS) patients. |
| 696 | 17211152 | Direct sequencing was performed after PCR amplification of all 29 and 8 exons of the NPHS1 and NPHS2 genes, respectively. |
| 697 | 17211152 | The results demonstrate that NPHS1 and NPHS2 mutations are also present in Chinese sporadic NS patients, suggesting that genetic changes of nephrin and podocin may play pathogenetic roles in some patients with sporadic steroid resistant NS. |
| 698 | 17211152 | NPHS1 and NPHS2 gene mutations in Chinese children with sporadic nephrotic syndrome. |
| 699 | 17211152 | Mutational analyses of NPHS1 and NPHS2 were performed to verify this hypothesis in sporadic nephrotic syndrome (NS) patients. |
| 700 | 17211152 | Direct sequencing was performed after PCR amplification of all 29 and 8 exons of the NPHS1 and NPHS2 genes, respectively. |
| 701 | 17211152 | The results demonstrate that NPHS1 and NPHS2 mutations are also present in Chinese sporadic NS patients, suggesting that genetic changes of nephrin and podocin may play pathogenetic roles in some patients with sporadic steroid resistant NS. |
| 702 | 17211152 | NPHS1 and NPHS2 gene mutations in Chinese children with sporadic nephrotic syndrome. |
| 703 | 17211152 | Mutational analyses of NPHS1 and NPHS2 were performed to verify this hypothesis in sporadic nephrotic syndrome (NS) patients. |
| 704 | 17211152 | Direct sequencing was performed after PCR amplification of all 29 and 8 exons of the NPHS1 and NPHS2 genes, respectively. |
| 705 | 17211152 | The results demonstrate that NPHS1 and NPHS2 mutations are also present in Chinese sporadic NS patients, suggesting that genetic changes of nephrin and podocin may play pathogenetic roles in some patients with sporadic steroid resistant NS. |
| 706 | 17255128 | Glomerular expression of nephrin and synaptopodin, but not podocin, is decreased in kidney sections from women with preeclampsia. |
| 707 | 17264876 | Reduction of VEGF-A and CTGF expression in diabetic nephropathy is associated with podocyte loss. |
| 708 | 17264876 | We now set out to investigate the relationship between reduced VEGF-A and connective tissue growth factor (CTGF) expression levels, the number of podocytes, and the extent of interstitial fibrosis. |
| 709 | 17264876 | Laser capture microdissection was applied to obtain glomerular RNA from 28 patients with DN and 22 controls. mRNA levels of VEGF-A, CTGF, nephrin, podocin, and Wilms tumor1 (WT1) were measured using real-time polymerase chain reaction. |
| 710 | 17264876 | Protein expression was evaluated using immuno-stainings for VEGF-A and CTGF, as well as markers for podocytes (WT1) and endothelial cells (CD31). |
| 711 | 17264876 | We found a significant decrease in glomerular mRNA levels for VEGF-A (2.5 times), CTGF (1.6), nephrin (2.8), podocin (3.3), and WT1 (1.7) in patients with DN. |
| 712 | 17264876 | There was a significant correlation between expression of podocyte markers and VEGF-A mRNA levels, and an inverse correlation between podocin message and the extent of interstitial fibrosis. |
| 713 | 17264876 | The results may suggest that downregulation of VEGF-A and CTGF in DN is a result of podocyte loss. |
| 714 | 17264876 | Reduction of VEGF-A and CTGF expression in diabetic nephropathy is associated with podocyte loss. |
| 715 | 17264876 | We now set out to investigate the relationship between reduced VEGF-A and connective tissue growth factor (CTGF) expression levels, the number of podocytes, and the extent of interstitial fibrosis. |
| 716 | 17264876 | Laser capture microdissection was applied to obtain glomerular RNA from 28 patients with DN and 22 controls. mRNA levels of VEGF-A, CTGF, nephrin, podocin, and Wilms tumor1 (WT1) were measured using real-time polymerase chain reaction. |
| 717 | 17264876 | Protein expression was evaluated using immuno-stainings for VEGF-A and CTGF, as well as markers for podocytes (WT1) and endothelial cells (CD31). |
| 718 | 17264876 | We found a significant decrease in glomerular mRNA levels for VEGF-A (2.5 times), CTGF (1.6), nephrin (2.8), podocin (3.3), and WT1 (1.7) in patients with DN. |
| 719 | 17264876 | There was a significant correlation between expression of podocyte markers and VEGF-A mRNA levels, and an inverse correlation between podocin message and the extent of interstitial fibrosis. |
| 720 | 17264876 | The results may suggest that downregulation of VEGF-A and CTGF in DN is a result of podocyte loss. |
| 721 | 17264876 | Reduction of VEGF-A and CTGF expression in diabetic nephropathy is associated with podocyte loss. |
| 722 | 17264876 | We now set out to investigate the relationship between reduced VEGF-A and connective tissue growth factor (CTGF) expression levels, the number of podocytes, and the extent of interstitial fibrosis. |
| 723 | 17264876 | Laser capture microdissection was applied to obtain glomerular RNA from 28 patients with DN and 22 controls. mRNA levels of VEGF-A, CTGF, nephrin, podocin, and Wilms tumor1 (WT1) were measured using real-time polymerase chain reaction. |
| 724 | 17264876 | Protein expression was evaluated using immuno-stainings for VEGF-A and CTGF, as well as markers for podocytes (WT1) and endothelial cells (CD31). |
| 725 | 17264876 | We found a significant decrease in glomerular mRNA levels for VEGF-A (2.5 times), CTGF (1.6), nephrin (2.8), podocin (3.3), and WT1 (1.7) in patients with DN. |
| 726 | 17264876 | There was a significant correlation between expression of podocyte markers and VEGF-A mRNA levels, and an inverse correlation between podocin message and the extent of interstitial fibrosis. |
| 727 | 17264876 | The results may suggest that downregulation of VEGF-A and CTGF in DN is a result of podocyte loss. |
| 728 | 17316599 | The podocyte-specific inactivation of Lmx1b, Ldb1 and E2a yields new insight into a transcriptional network in podocytes. |
| 729 | 17316599 | Promising candidates for modifier proteins are the proteins interacting with LMX1B, such as LDB1 and E47. |
| 730 | 17316599 | In contrast to findings in these mice, however, in which a downregulation of the Col4a3, Col4a4 and Nphs2 genes has been described, no such changes have been detected in kidney biopsies from patients. |
| 731 | 17316599 | We now report on our results on the characterization of constitutive podocyte-specific Lmx1b, Ldb1 and E2a knock-out mice. |
| 732 | 17316599 | Constitutive podocyte-specific Lmx1b knock-out mice survive for approximately 2 weeks after birth and do not present with a downregulation of the Col4a3, Col4a4 and Nphs2 genes, therefore they mimic the human disease more closely. |
| 733 | 17316599 | The podocyte-specific Ldb1 knock-out mice survive longer, but then also succumb to renal failure, whereas the E2a knock-out mice show no renal symptoms for at least 6 months after birth. |
| 734 | 17316599 | We conclude that LDB1, but not E2A is a promising candidate as a modifier gene in patients with nail-patella syndrome. |
| 735 | 17316599 | The podocyte-specific inactivation of Lmx1b, Ldb1 and E2a yields new insight into a transcriptional network in podocytes. |
| 736 | 17316599 | Promising candidates for modifier proteins are the proteins interacting with LMX1B, such as LDB1 and E47. |
| 737 | 17316599 | In contrast to findings in these mice, however, in which a downregulation of the Col4a3, Col4a4 and Nphs2 genes has been described, no such changes have been detected in kidney biopsies from patients. |
| 738 | 17316599 | We now report on our results on the characterization of constitutive podocyte-specific Lmx1b, Ldb1 and E2a knock-out mice. |
| 739 | 17316599 | Constitutive podocyte-specific Lmx1b knock-out mice survive for approximately 2 weeks after birth and do not present with a downregulation of the Col4a3, Col4a4 and Nphs2 genes, therefore they mimic the human disease more closely. |
| 740 | 17316599 | The podocyte-specific Ldb1 knock-out mice survive longer, but then also succumb to renal failure, whereas the E2a knock-out mice show no renal symptoms for at least 6 months after birth. |
| 741 | 17316599 | We conclude that LDB1, but not E2A is a promising candidate as a modifier gene in patients with nail-patella syndrome. |
| 742 | 17348483 | Investigation of the different proteins revealed that the lack of nephrin and podocin is the leading cause of several inherited forms of proteinuria. |
| 743 | 17429054 | Serum IL-13, albumin, cholesterol, and creatinine and urine albumin were measured serially. |
| 744 | 17429054 | Glomerular gene expression of nephrin, podocin, dystroglycan, B7-1, and IL-13 receptor subunits were examined using real-time PCR with hybridization probes and expressed as an index against beta-actin. |
| 745 | 17429054 | Glomerular gene expression was significantly upregulated for B7-1, IL-4Ralpha, and IL-13Ralpha2 but downregulated for nephrin, podocin, and dystroglycan. |
| 746 | 17429054 | Immunofluorescence staining intensity was reduced for nephrin, podocin, and dystroglycan but increased for B7-1 and IL-4Ralpha in IL-13-transfected rats compared with controls. |
| 747 | 17429054 | In conclusion, these results suggest that IL-13 overexpression in the rat could lead to podocyte injury with downregulation of nephrin, podocin, and dystroglycan and a concurrent upregulation of B7-1 in the glomeruli, inducing a minimal change-like nephropathy that is characterized by increased proteinuria, hypoalbuminemia, hypercholesterolemia, and fusion of podocyte foot processes. |
| 748 | 17429054 | Serum IL-13, albumin, cholesterol, and creatinine and urine albumin were measured serially. |
| 749 | 17429054 | Glomerular gene expression of nephrin, podocin, dystroglycan, B7-1, and IL-13 receptor subunits were examined using real-time PCR with hybridization probes and expressed as an index against beta-actin. |
| 750 | 17429054 | Glomerular gene expression was significantly upregulated for B7-1, IL-4Ralpha, and IL-13Ralpha2 but downregulated for nephrin, podocin, and dystroglycan. |
| 751 | 17429054 | Immunofluorescence staining intensity was reduced for nephrin, podocin, and dystroglycan but increased for B7-1 and IL-4Ralpha in IL-13-transfected rats compared with controls. |
| 752 | 17429054 | In conclusion, these results suggest that IL-13 overexpression in the rat could lead to podocyte injury with downregulation of nephrin, podocin, and dystroglycan and a concurrent upregulation of B7-1 in the glomeruli, inducing a minimal change-like nephropathy that is characterized by increased proteinuria, hypoalbuminemia, hypercholesterolemia, and fusion of podocyte foot processes. |
| 753 | 17429054 | Serum IL-13, albumin, cholesterol, and creatinine and urine albumin were measured serially. |
| 754 | 17429054 | Glomerular gene expression of nephrin, podocin, dystroglycan, B7-1, and IL-13 receptor subunits were examined using real-time PCR with hybridization probes and expressed as an index against beta-actin. |
| 755 | 17429054 | Glomerular gene expression was significantly upregulated for B7-1, IL-4Ralpha, and IL-13Ralpha2 but downregulated for nephrin, podocin, and dystroglycan. |
| 756 | 17429054 | Immunofluorescence staining intensity was reduced for nephrin, podocin, and dystroglycan but increased for B7-1 and IL-4Ralpha in IL-13-transfected rats compared with controls. |
| 757 | 17429054 | In conclusion, these results suggest that IL-13 overexpression in the rat could lead to podocyte injury with downregulation of nephrin, podocin, and dystroglycan and a concurrent upregulation of B7-1 in the glomeruli, inducing a minimal change-like nephropathy that is characterized by increased proteinuria, hypoalbuminemia, hypercholesterolemia, and fusion of podocyte foot processes. |
| 758 | 17429054 | Serum IL-13, albumin, cholesterol, and creatinine and urine albumin were measured serially. |
| 759 | 17429054 | Glomerular gene expression of nephrin, podocin, dystroglycan, B7-1, and IL-13 receptor subunits were examined using real-time PCR with hybridization probes and expressed as an index against beta-actin. |
| 760 | 17429054 | Glomerular gene expression was significantly upregulated for B7-1, IL-4Ralpha, and IL-13Ralpha2 but downregulated for nephrin, podocin, and dystroglycan. |
| 761 | 17429054 | Immunofluorescence staining intensity was reduced for nephrin, podocin, and dystroglycan but increased for B7-1 and IL-4Ralpha in IL-13-transfected rats compared with controls. |
| 762 | 17429054 | In conclusion, these results suggest that IL-13 overexpression in the rat could lead to podocyte injury with downregulation of nephrin, podocin, and dystroglycan and a concurrent upregulation of B7-1 in the glomeruli, inducing a minimal change-like nephropathy that is characterized by increased proteinuria, hypoalbuminemia, hypercholesterolemia, and fusion of podocyte foot processes. |
| 763 | 17457373 | Upregulation of B7.1 with the downregulation of GLEPP1, Wilms' tumor gene (WT1), megalin, and vascular endothelial growth factor started early and persisted through the course of disease. |
| 764 | 17457373 | In the puromycin and the combined models, changes in GLEPP1 expression were corticosteroid-sensitive, whereas B7.1, WT1, vascular endothelial growth factor, and most slit diaphragm genes involved later in the combined model, except podocin, were corticosteroid-resistant. |
| 765 | 17457373 | There was a very early increase in the nuclear expression of podocyte transcription factors ZHX2 and ZHX1 that may be linked to the changes in gene expression in the combined proteinuric model. |
| 766 | 17459670 | TRPC6 and FSGS: the latest TRP channelopathy. |
| 767 | 17459670 | Resultant to these pursuits, several podocyte structural proteins such as nephrin, podocin, alpha-actinin 4 (ACTN4), and CD2-associated protein (CD2AP) have emerged to provide critical insight into the pathogenesis of hereditary nephrotic syndromes. |
| 768 | 17459670 | The latest advance in familial FSGS has been the discovery of a mutant form of canonical transient receptor potential cation channel 6 (TRPC6), which causes an increase in calcium transients and essentially a gain of function in this cation channel located on the podocyte cell membrane. |
| 769 | 17459670 | TRPC6 channels have been shown to be activated via phospholipase C stimulation. |
| 770 | 17459670 | Mutant TRPC6 may also amplify injurious signals mediated by Ang II, a common final pathway of podocyte apoptosis in various mammalian species. |
| 771 | 17459670 | Current evidence also suggests that blocking TRPC6 channels may be of therapeutic benefit in idiopathic FSGS, a disease with a generally poor prognosis. |
| 772 | 17459670 | This creates the exciting possibility that blocking TRPC6 channels within the podocyte may translate into long-lasting clinical benefits in patients with FSGS. |
| 773 | 17530296 | Renin-angiotensin axis blockade reduces proteinuria in presymptomatic patients with familial FSGS. |
| 774 | 17530296 | Familial and genetic forms of focal segmental glomerulosclerosis (FSGS) are associated with six different mutations in genes affecting the podocyte (NPHS2, ACTN4, CD2AP, WT1, TRPC6, and PLCE1). |
| 775 | 17530296 | We describe three children from two different families with familial FSGS in whom partial to complete remission of proteinuria was attained through early blockade of the renin-angiotensin axis. |
| 776 | 17530296 | We speculate that presymptomatic patients with normal renal function who have genetic or familial FSGS may benefit from early blockade of the renin-angiotensin axis and that this may also prevent progressive renal disease. |
| 777 | 17570936 | In the context of the slit diaphragm signaling network, TRPC6 is clustered and regulated by a podocin-lipid complex that might translate mechanical tension to ion channel action. |
| 778 | 17675666 | Under nephrotic conditions,however, foot process effacement leads to the loss of slit diaphragms and the new formationof tight junctions composed of the proteins coxsackievirus and adenovirus receptor (CAR) and zonula occludens 1 (ZO-1). |
| 779 | 17675666 | In this study, we confirmed that podocin colocalizes with CAR and ZO-1 at the tight junction between foot processes in nephrotic rats. |
| 780 | 17675666 | Using primary cultures of rat podocytes, as well as cell lines that co-expressed podocin and CAR, we observed that podocin was recruited to sites of cell-cell contact and that it co-localized with CAR and ZO-1. |
| 781 | 17675666 | Consistent with this, we found that podociin facilitated the coalescence of preassembled lipid rafts containing CAR and restricted their lateral mobility, the latter likely a result of dynamic actin reorganization and subsequent tethering of CAR-podocin complexes to the cytoskeleton. |
| 782 | 17675666 | Under nephrotic conditions,however, foot process effacement leads to the loss of slit diaphragms and the new formationof tight junctions composed of the proteins coxsackievirus and adenovirus receptor (CAR) and zonula occludens 1 (ZO-1). |
| 783 | 17675666 | In this study, we confirmed that podocin colocalizes with CAR and ZO-1 at the tight junction between foot processes in nephrotic rats. |
| 784 | 17675666 | Using primary cultures of rat podocytes, as well as cell lines that co-expressed podocin and CAR, we observed that podocin was recruited to sites of cell-cell contact and that it co-localized with CAR and ZO-1. |
| 785 | 17675666 | Consistent with this, we found that podociin facilitated the coalescence of preassembled lipid rafts containing CAR and restricted their lateral mobility, the latter likely a result of dynamic actin reorganization and subsequent tethering of CAR-podocin complexes to the cytoskeleton. |
| 786 | 17675666 | Under nephrotic conditions,however, foot process effacement leads to the loss of slit diaphragms and the new formationof tight junctions composed of the proteins coxsackievirus and adenovirus receptor (CAR) and zonula occludens 1 (ZO-1). |
| 787 | 17675666 | In this study, we confirmed that podocin colocalizes with CAR and ZO-1 at the tight junction between foot processes in nephrotic rats. |
| 788 | 17675666 | Using primary cultures of rat podocytes, as well as cell lines that co-expressed podocin and CAR, we observed that podocin was recruited to sites of cell-cell contact and that it co-localized with CAR and ZO-1. |
| 789 | 17675666 | Consistent with this, we found that podociin facilitated the coalescence of preassembled lipid rafts containing CAR and restricted their lateral mobility, the latter likely a result of dynamic actin reorganization and subsequent tethering of CAR-podocin complexes to the cytoskeleton. |
| 790 | 17694336 | The expression of podocyte molecules (WT1, nephrin, podocin, alpha-actinin 4 and CD2AP) were also investigated in a renal specimen of this FS patient. |
| 791 | 17699558 | In addition, after knockdown of CD2-associated protein (CD2AP) and podocin, two well-characterized genetic contributors to podocyte differentiation in mammals, we observed glomerular loss of serum macromolecules similar to that seen in mammalian kidneys with inborn mutations in these genes. |
| 792 | 17804487 | High glucose (HG; 25 mM) induces rounding of differentiated podocytes and changes in the distribution of F-actin but without quantitative changes in E-cadherin and the podocyte markers podocin, CD2AP, Neph1, or synaptopodin. |
| 793 | 17804487 | In these cells, BMP7 effectively activates smad5 (but not smad1) and raises p38 phosphorylation [which is also increased by transforming growth factor-beta (TGF-beta)]. |
| 794 | 17804487 | HG as well as TGF-beta raise caspase-3 activity, increase apoptosis, and reduce cell survival which is, in part, blocked by BMP7. |
| 795 | 17804487 | Knockdown and forced expression studies indicate that smad5 is required as well as sufficient for these actions of BMP7. |
| 796 | 17804487 | These findings indicate that BMP7 is a differentiation and survival factor for podocytes, requires smad5, and can reduce diabetic podocyte injury. |
| 797 | 18033240 | We studied the role of phosphoinositide 3-kinase (PI3K), activated via the phosphorylation of nephrin, in actin cytoskeletal reorganization of cultured rat podocytes. |
| 798 | 18033240 | Phosphorylation of rat nephrin by the Fyn kinase markedly increased its interaction with a regulatory subunit of PI3K. |
| 799 | 18033240 | Stable transfection of rat nephrin in the podocytes with podocin led to nephrin tyrosine phosphorylation, PI3K-dependent phosphorylation of Akt, increased Rac1 activity, and an altered actin cytoskeleton with decreased stress fibers and increased lamellipodia. |
| 800 | 18033240 | These changes were reversed with an inhibitor of PI3K and not seen when the nephrin-mutant Y1152F replaced wild-type nephrin. |
| 801 | 18033240 | Rac1 and Akt1 contributed to lamellipodia formation and decreased stress fibers, respectively. |
| 802 | 18033240 | Finally, in the rat model of puromycin aminonucleoside nephrosis, nephrin tyrosine phosphorylation, nephrin-PI3K association, and glomerular Akt phosphorylation were all decreased. |
| 803 | 18033240 | Our results suggest that PI3K is involved in nephrin-mediated actin reorganization in podocytes. |
| 804 | 18075495 | Here, we show that exogenous semaphorin3a caused acute nephrotic range proteinuria associated with podocyte foot process effacement and fusion, endothelial cell damage, decreased vascular endothelial growth factor-A receptor expression, and downregulation of the slit-diaphragm proteins podocin, nephrin, and CD2-associated protein. |
| 805 | 18075495 | When vascular endothelial growth factor 165 was administered at the same time as Semaphorin3a, no proteinuria or renal ultrastructural abnormalities occurred, suggesting that semaphorin3a effects may be mediated, in part, by downregulation of vascular endothelial growth factor receptor 2 signaling. |
| 806 | 18082680 | Mice with podocyte specific deletion of integrin beta1 (podocin-Cre beta1-fl/fl mice) are born normal but cannot complete postnatal renal development. |
| 807 | 18082680 | The integrin linked kinase (ILK) is a downstream mediator of integrin beta1 activity in epithelial cells. |
| 808 | 18082680 | To further explore whether integrin beta1-mediated signaling facilitates proper glomerular filtration, we generated mice deficient of ILK in the podocytes (podocin-Cre ILK-fl/fl mice). |
| 809 | 18082680 | Mice with podocyte specific deletion of integrin beta1 (podocin-Cre beta1-fl/fl mice) are born normal but cannot complete postnatal renal development. |
| 810 | 18082680 | The integrin linked kinase (ILK) is a downstream mediator of integrin beta1 activity in epithelial cells. |
| 811 | 18082680 | To further explore whether integrin beta1-mediated signaling facilitates proper glomerular filtration, we generated mice deficient of ILK in the podocytes (podocin-Cre ILK-fl/fl mice). |
| 812 | 18253764 | These characteristic symptoms are caused by mutations in the gene encoding the transcription factor LMX1B, a member of the LIM-homeodomain gene family. |
| 813 | 18253764 | In contrast, however, podocin and the alpha3 and alpha4 chains of collagen IV are absent in the glomeruli of Lmx1b knockout mice. |
| 814 | 18287402 | Preeclamptic sera induce nephrin shedding from podocytes through endothelin-1 release by endothelial glomerular cells. |
| 815 | 18287402 | In contrast, conditioned medium obtained from glomerular endothelial cells incubated with PE sera induced loss of nephrin and synaptopodin, but not of podocin, from podocytes. |
| 816 | 18287402 | Studies with an endothelin-1 (ET-1) receptor antagonist that abrogated the loss of nephrin triggered by glomerular endothelial conditioned medium of PE sera indicated that ET-1 was the main effector of nephrin loss. |
| 817 | 18287402 | Indeed, ET-1 was synthesized and released from glomerular endothelial cells when incubated with PE sera, and recombinant ET-1 triggered nephrin shedding from podocytes. |
| 818 | 18287402 | Moreover, VEGF blockade induced ET-1 release from endothelial cells, and in turn the conditioned medium obtained triggered nephrin loss. |
| 819 | 18288100 | Gene expression profiling revealed marked differences between these and the podocin-null mice, including significant perturbations of podocyte-expressed genes such as Cd2ap, Vegfa and the transcription factors Lmx1b and Zhx2. |
| 820 | 18288100 | Upregulation of Serpine1 and Tgfb1 implicates these as potential mediators of disease progression in these mice. |
| 821 | 18337488 | Features of mature podocytes were lost: Foot processes were effaced; expression of Wt1, Nphs1, and Nphs2 was downregulated; cell-cycle re-entry was induced; and the expression of Pax2 was increased. |
| 822 | 18364721 | Candidate genes so far identified in renal disease include those encoding the podocyte proteins nephrin and podocin, the transcription factor WT1, the calcium channel TRPC6 and the enzyme phospholipase C-epsilon-1 (in congenital nephrotic syndrome and focal segmental glomerulosclerosis), and carnosinase (in diabetic nephropathy). |
| 823 | 18437205 | Primary coenzyme Q deficiency in Pdss2 mutant mice causes isolated renal disease. |
| 824 | 18437205 | Its multi-step biosynthesis involves production of polyisoprenoid diphosphate in a reaction that requires the enzymes be encoded by PDSS1 and PDSS2. |
| 825 | 18437205 | Disease manifestations originate specifically in glomerular podocytes, as renal disease is seen in Podocin/cre,Pdss2(loxP/loxP) knockout mice but not in conditional knockouts targeted to renal tubular epithelium, monocytes, or hepatocytes. |
| 826 | 18437205 | Liver-conditional B6.Alb/cre,Pdss2(loxP/loxP) knockout mice have no overt disease despite demonstration that their livers have undetectable CoQ9 levels, impaired respiratory capacity, and significantly altered intermediary metabolism as evidenced by transcriptional profiling and amino acid quantitation. |
| 827 | 18462046 | The most common mutations are in 4 genes, 3 of which are podocyte genes: NPHS1 (Finnish nephropathy), NPHS2 (podocin-induced focal segmental glomerulosclerosis), WT1 (diffuse mesangial sclerosis), and LAMB2 (Pierson syndrome). |
| 828 | 18509322 | The antiproteinuric effect was associated with improvement in the foot process effacement, a decrease in the podocyte injury marker desmin as well as the restoration of nephrin and podocin expression and distribution. |
| 829 | 18509322 | In cultured mouse podocytes triptolide pretreatment prevented the puromycin-induced disruption of the actin cytoskeleton and microfilament-associated synaptopodin while protecting nephrin and podocin expression. |
| 830 | 18509322 | The antiproteinuric effect was associated with improvement in the foot process effacement, a decrease in the podocyte injury marker desmin as well as the restoration of nephrin and podocin expression and distribution. |
| 831 | 18509322 | In cultured mouse podocytes triptolide pretreatment prevented the puromycin-induced disruption of the actin cytoskeleton and microfilament-associated synaptopodin while protecting nephrin and podocin expression. |
| 832 | 18535845 | Although LMX1B is a developmental LIM-homeodomain transcription factor, it is expressed in post-natal life in the glomerular podocyte, suggesting a regulatory role in that cell. |
| 833 | 18535845 | NPHS2, CD2AP), the transription of which is regulated by LMX1B. |
| 834 | 18715943 | The staining of the SD molecules nephrin, podocin, and NEPH1 had already shifted to a discontinuous dotlike pattern at the initiation phase of the disease, when neither proteinuria nor any morphological alterations were detected yet. |
| 835 | 18715943 | On day 28, when severe proteinuria was detected and sclerotic changes were already observed, alteration of the expressions of nephrin, podocin, and NEPH1 worsened, but no alteration in the expression of other SD-associated molecules or other podocyte molecules was detected. |
| 836 | 18715943 | The staining of the SD molecules nephrin, podocin, and NEPH1 had already shifted to a discontinuous dotlike pattern at the initiation phase of the disease, when neither proteinuria nor any morphological alterations were detected yet. |
| 837 | 18715943 | On day 28, when severe proteinuria was detected and sclerotic changes were already observed, alteration of the expressions of nephrin, podocin, and NEPH1 worsened, but no alteration in the expression of other SD-associated molecules or other podocyte molecules was detected. |
| 838 | 18809387 | Activated macrophages down-regulate podocyte nephrin and podocin expression via stress-activated protein kinases. |
| 839 | 18809387 | The development of proteinuria and glomerulosclerosis in kidney disease is associated with podocyte damage, including down-regulation of nephrin and podocin. |
| 840 | 18809387 | Conditioned media (CM) from activated macrophages caused a 50-60% reduction in nephrin and podocin mRNA and protein expression in cultured mouse podocytes and rat glomeruli. |
| 841 | 18809387 | The addition of recombinant TNFalpha to podocytes or glomeruli caused a comparable reduction in podocyte nephrin and podocin expression to that of macrophage CM. |
| 842 | 18809387 | Inhibition of c-Jun amino terminal kinase (JNK) or p38 kinase abolished the TNFalpha-induced reduction in nephrin and podocin expression. |
| 843 | 18809387 | This may explain, in part, the protective effects of JNK and p38 blockade in experimental kidney disease. |
| 844 | 18809387 | Activated macrophages down-regulate podocyte nephrin and podocin expression via stress-activated protein kinases. |
| 845 | 18809387 | The development of proteinuria and glomerulosclerosis in kidney disease is associated with podocyte damage, including down-regulation of nephrin and podocin. |
| 846 | 18809387 | Conditioned media (CM) from activated macrophages caused a 50-60% reduction in nephrin and podocin mRNA and protein expression in cultured mouse podocytes and rat glomeruli. |
| 847 | 18809387 | The addition of recombinant TNFalpha to podocytes or glomeruli caused a comparable reduction in podocyte nephrin and podocin expression to that of macrophage CM. |
| 848 | 18809387 | Inhibition of c-Jun amino terminal kinase (JNK) or p38 kinase abolished the TNFalpha-induced reduction in nephrin and podocin expression. |
| 849 | 18809387 | This may explain, in part, the protective effects of JNK and p38 blockade in experimental kidney disease. |
| 850 | 18809387 | Activated macrophages down-regulate podocyte nephrin and podocin expression via stress-activated protein kinases. |
| 851 | 18809387 | The development of proteinuria and glomerulosclerosis in kidney disease is associated with podocyte damage, including down-regulation of nephrin and podocin. |
| 852 | 18809387 | Conditioned media (CM) from activated macrophages caused a 50-60% reduction in nephrin and podocin mRNA and protein expression in cultured mouse podocytes and rat glomeruli. |
| 853 | 18809387 | The addition of recombinant TNFalpha to podocytes or glomeruli caused a comparable reduction in podocyte nephrin and podocin expression to that of macrophage CM. |
| 854 | 18809387 | Inhibition of c-Jun amino terminal kinase (JNK) or p38 kinase abolished the TNFalpha-induced reduction in nephrin and podocin expression. |
| 855 | 18809387 | This may explain, in part, the protective effects of JNK and p38 blockade in experimental kidney disease. |
| 856 | 18809387 | Activated macrophages down-regulate podocyte nephrin and podocin expression via stress-activated protein kinases. |
| 857 | 18809387 | The development of proteinuria and glomerulosclerosis in kidney disease is associated with podocyte damage, including down-regulation of nephrin and podocin. |
| 858 | 18809387 | Conditioned media (CM) from activated macrophages caused a 50-60% reduction in nephrin and podocin mRNA and protein expression in cultured mouse podocytes and rat glomeruli. |
| 859 | 18809387 | The addition of recombinant TNFalpha to podocytes or glomeruli caused a comparable reduction in podocyte nephrin and podocin expression to that of macrophage CM. |
| 860 | 18809387 | Inhibition of c-Jun amino terminal kinase (JNK) or p38 kinase abolished the TNFalpha-induced reduction in nephrin and podocin expression. |
| 861 | 18809387 | This may explain, in part, the protective effects of JNK and p38 blockade in experimental kidney disease. |
| 862 | 18809387 | Activated macrophages down-regulate podocyte nephrin and podocin expression via stress-activated protein kinases. |
| 863 | 18809387 | The development of proteinuria and glomerulosclerosis in kidney disease is associated with podocyte damage, including down-regulation of nephrin and podocin. |
| 864 | 18809387 | Conditioned media (CM) from activated macrophages caused a 50-60% reduction in nephrin and podocin mRNA and protein expression in cultured mouse podocytes and rat glomeruli. |
| 865 | 18809387 | The addition of recombinant TNFalpha to podocytes or glomeruli caused a comparable reduction in podocyte nephrin and podocin expression to that of macrophage CM. |
| 866 | 18809387 | Inhibition of c-Jun amino terminal kinase (JNK) or p38 kinase abolished the TNFalpha-induced reduction in nephrin and podocin expression. |
| 867 | 18809387 | This may explain, in part, the protective effects of JNK and p38 blockade in experimental kidney disease. |
| 868 | 18832437 | Expression of the slit diaphragm proteins nephrin and podocin was decreased, and expression of the transcription factor WT1 was relatively unaffected. |
| 869 | 18971929 | We find that fly (Drosophila melanogaster) orthologues of the major constituents of the slit diaphragm, including nephrin, NEPH1 (also known as KIRREL), CD2AP, ZO-1 (TJP1) and podocin, are expressed in the nephrocyte and form a complex of interacting proteins that closely mirrors the vertebrate slit diaphragm complex. |
| 870 | 18971929 | Furthermore, we find that the nephrocyte diaphragm is completely lost in flies lacking the orthologues of nephrin or NEPH1-a phenotype resembling loss of the slit diaphragm in the absence of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1. |
| 871 | 19142224 | The nephrin-podocin complex is the main constituent of slit diaphragms. |
| 872 | 19142224 | Here, we demonstrate that the PAR3-atypical protein kinase C (aPKC)-PAR6beta cell polarity proteins co-localize to the slit diaphragms with nephrin. |
| 873 | 19142224 | The aPKC-PAR3 complex associates with the nephrin-podocin complex in podocytes through direct interaction between PAR3 and nephrin, and the kinase activity of aPKC is required for the appropriate distribution of nephrin and podocin in podocytes. |
| 874 | 19142224 | The nephrin-podocin complex is the main constituent of slit diaphragms. |
| 875 | 19142224 | Here, we demonstrate that the PAR3-atypical protein kinase C (aPKC)-PAR6beta cell polarity proteins co-localize to the slit diaphragms with nephrin. |
| 876 | 19142224 | The aPKC-PAR3 complex associates with the nephrin-podocin complex in podocytes through direct interaction between PAR3 and nephrin, and the kinase activity of aPKC is required for the appropriate distribution of nephrin and podocin in podocytes. |
| 877 | 19261739 | Recent evidence suggests that mineralocorticoid receptor (MR) antagonism has beneficial effects on tissue oxidative stress and insulin metabolic signaling as well as reducing proteinuria. |
| 878 | 19261739 | However, the mechanisms by which MR antagonism corrects both renin-angiotensin-aldosterone system (RAAS) impairments in renal insulin metabolic signaling and filtration barrier/podocyte injury remain unknown. |
| 879 | 19261739 | Albuminuria, podocyte-specific proteins (synaptopodin, nephrin, and podocin), and ultrastructural analysis of the glomerular filtration barrier were measured in relation to RAAS activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, reactive oxygen species (ROS), and the redox-sensitive Rho kinase (ROK). |
| 880 | 19261739 | Insulin metabolic signaling was determined via measurement of insulin receptor substrate-1 (IRS-1) phosphorylation, IRS-1 ubiquitin/proteasomal degradation, and phosphorylation of Akt. |
| 881 | 19261739 | Ren2 rats exhibited albuminuria, loss of podocyte-specific proteins, and podocyte foot process effacement contemporaneous with reduced renal IRS-1 and protein kinase B/Akt phosphorylation compared with SD control rats (each P < 0.05). |
| 882 | 19261739 | Ren2 kidneys also manifested increased NADPH oxidase/ROS/ROK in conjunction with enhanced renal tissue levels of angiotensin II (ANG II), ANG-(1-12), and angiotensin type 1 receptor. |
| 883 | 19261739 | Low-dose spironolactone treatment reduced albuminuria and tissue RAAS activity and improved podocyte structural and protein integrity with improvements in IRS-1/Akt phosphorylation. |
| 884 | 19266252 | Some recent studies demonstrated that podocin, CD2-associated protein and NEPH1 are also functional molecules in the slit diaphragm, and their expressions are altered in membranous nephropathy and also in focal glomerulosclerosis. |
| 885 | 19342370 | Moreover, the preserved podocyte number in SPARC(-/-) mice correlates with reduced urinary levels of both nephrin and podocin. |
| 886 | 19478094 | Slit diaphragms, considered specialized adherens junctions, contain both unique membrane proteins (e.g., nephrin, podocin, and Neph1) and typical adherens junction proteins (e.g., P-cadherin, FAT, and catenins). |
| 887 | 19478094 | Here, immunofluorescence, immunogold labeling, and cell fractionation demonstrated that rat slit diaphragms contain the tight junction proteins JAM-A (junctional adhesion molecule A), occludin, and cingulin. |
| 888 | 19478094 | We found these proteins in the same protein complexes as nephrin, podocin, CD2AP, ZO-1, and Neph1 by cosedimentation, coimmunoprecipitation, and pull-down assays. |
| 889 | 19478094 | PAN nephrosis increased the protein levels of JAM-A, occludin, cingulin, and ZO-1 several-fold in glomeruli and loosened their attachment to the actin cytoskeleton. |
| 890 | 19478094 | Slit diaphragms, considered specialized adherens junctions, contain both unique membrane proteins (e.g., nephrin, podocin, and Neph1) and typical adherens junction proteins (e.g., P-cadherin, FAT, and catenins). |
| 891 | 19478094 | Here, immunofluorescence, immunogold labeling, and cell fractionation demonstrated that rat slit diaphragms contain the tight junction proteins JAM-A (junctional adhesion molecule A), occludin, and cingulin. |
| 892 | 19478094 | We found these proteins in the same protein complexes as nephrin, podocin, CD2AP, ZO-1, and Neph1 by cosedimentation, coimmunoprecipitation, and pull-down assays. |
| 893 | 19478094 | PAN nephrosis increased the protein levels of JAM-A, occludin, cingulin, and ZO-1 several-fold in glomeruli and loosened their attachment to the actin cytoskeleton. |
| 894 | 19562271 | The transcriptional regulation of podocin (NPHS2) by Lmx1b and a promoter single nucleotide polymorphism. |
| 895 | 19562271 | Our data shows that the transcription of podocin is mainly regulated by the transcription factor Lmx1b, which binds to a FLAT-F element and displays enhancer function. |
| 896 | 19562271 | Our data indicates that among other factors, podocin is specifically regulated by the transcription factor Lmx1b and by the functional polymorphism -116C/T. |
| 897 | 19562271 | The transcriptional regulation of podocin (NPHS2) by Lmx1b and a promoter single nucleotide polymorphism. |
| 898 | 19562271 | Our data shows that the transcription of podocin is mainly regulated by the transcription factor Lmx1b, which binds to a FLAT-F element and displays enhancer function. |
| 899 | 19562271 | Our data indicates that among other factors, podocin is specifically regulated by the transcription factor Lmx1b and by the functional polymorphism -116C/T. |
| 900 | 19562271 | The transcriptional regulation of podocin (NPHS2) by Lmx1b and a promoter single nucleotide polymorphism. |
| 901 | 19562271 | Our data shows that the transcription of podocin is mainly regulated by the transcription factor Lmx1b, which binds to a FLAT-F element and displays enhancer function. |
| 902 | 19562271 | Our data indicates that among other factors, podocin is specifically regulated by the transcription factor Lmx1b and by the functional polymorphism -116C/T. |
| 903 | 19562370 | Here, we describe already well-characterized genetic diseases due to mutations in nephrin, podocin, CD2AP, alpha-actinin-4, WT1, and laminin beta2 chain, as well as more recently identified genetic abnormalities in TRPC6, phospholipase C epsilon, and the proteins encoded by the mitochondrial genome. |
| 904 | 19579288 | We found that human glomeruli deprived of the Bowman's capsule contain a population of CD133+CD146+ cells and a population of CD133-CD146+ cells expressing mesenchymal stem cell (MSC) markers and renal stem cell markers CD24 and Pax-2. |
| 905 | 19579288 | The CD133+CD146+ cells differed from those previously isolated from Bowman's capsule as they co-expressed endothelial markers, such as CD31 and von Willebrand factor (vWF), were CD24-negative and were not clonogenic, suggesting an endothelial commitment. |
| 906 | 19579288 | In addition to osteogenic, adipogenic, and chondrogenic differentiation, these cells were able to differentiate to endothelial cells and epithelial cells expressing podocytes markers such as nephrin, podocin, and synaptopodin. |
| 907 | 19579288 | Moreover, Gl-MSC when cultured in appropriate conditions, acquired mesangial cell markers such as alpha-smooth muscle actin (alpha-SMA) and angiotensin II (AT-II) receptor I. |
| 908 | 19816391 | Molecules like nephrin and podocin are directly involved in the formation of the slit diaphragm located at the end of the foot processes. |
| 909 | 19838659 | Here, we have addressed the role of alpha- and beta-adducin on glomerular function and disease using beta-adducin null mice, congenic substrains for alpha- and beta-adducin from the Milan hypertensive (MHS) and Milan normotensive (MNS) rats and patients with IgA nephropathy. |
| 910 | 19838659 | Targeted deletion of beta-adducin in mice reduced urinary protein excretion, preceded by an increase of podocyte protein expression (phospho-nephrin, synaptopodin, alpha-actinin, ZO-1, Fyn). |
| 911 | 19838659 | The introgression of polymorphic MHS beta-adducin locus into MNS (Add2, 529R) rats was associated with an early reduction of podocyte protein expression (nephrin, synaptopodin, alpha-actinin, ZO-1, podocin, Fyn), followed by severe glomerular and interstitial lesions and increased urinary protein excretion. |
| 912 | 19838659 | In patients with IgA nephropathy, the rate of decline of renal function over time was associated to polymorphic beta-adducin (ADD2, 1797T, rs4984) with a significant interaction with alpha-adducin (ADD1, 460W, rs4961). |
| 913 | 19850954 | Nephrin constituted a stable, signaling-competent microdomain through interaction with Fyn, a Src kinase, and podocin, a scaffold protein. |
| 914 | 19956976 | Analysis of recessive CD2AP and ACTN4 mutations in steroid-resistant nephrotic syndrome. |
| 915 | 19956976 | Based on the phenotype of Actn4 and Cd2ap null mice, we aimed to define the role of recessive CD2AP and ACTN4 mutations in a cohort of children with SRNS for which NPHS1, NPHS2, and PLCE1 mutations had been previously excluded. |
| 916 | 19956976 | CD2AP and ACTN4 mutational analysis was performed in 42 children from 35 unrelated families. |
| 917 | 19956976 | Recessive CD2AP and ACTN4 mutations are rare in children with SRNS. |
| 918 | 20031026 | This study demonstrates that the expression of the mesenchymal markers CD29 and CD44, the epithelial markers CD51 and ZO-1 and the podocyte markers CD2AP and NPHS2 can be induced in these cells via incubation with epidermal growth factor/platelet-derived growth factor BB and fibroblast growth factor 4/hepatocyte growth factor, respectively. |
| 919 | 20036696 | In the present study, we first demonstrated that an intact NADPH oxidase system is present in podocytes as shown by detection of its membrane subunit (gp91(phox)) and cytosolic subunit (p47(phox)). |
| 920 | 20036696 | Then, confocal microscopy showed that gp91(phox) and p47(phox) could be aggregated in lipid raft (LR) clusters in podocytes treated with homocysteine (Hcys), which were illustrated by their colocalization with cholera toxin B, a common LR marker. |
| 921 | 20036696 | By flotation of detergent-resistant membrane fractions we found that gp91(phox) and p47(phox) were enriched in LR fractions upon Hcys stimulation, and such enrichment of NADPH oxidase subunits and increase in its enzyme activity were blocked by MCD or filipin. |
| 922 | 20036696 | Functionally, disruption of LR clustering significantly attenuated Hcys-induced podocyte injury, as shown by their inhibitory effects on Hcys-decreased expression of slit diaphragm molecules such as nephrin and podocin. |
| 923 | 20375116 | Therefore, we generated two podocyte-specific GLUT1 transgenic mouse lines (driven by a podocin promoter) on a db/m C57BLKS background. |
| 924 | 20375116 | Levels of nephrin, neph1, CD2AP, podocin, and GLUT4 were not significantly different in transgenic compared with wild-type mice. |
| 925 | 20375116 | Taken together, increased podocyte GLUT1 expression in diabetic mice does not contribute to early diabetic nephropathy; surprisingly, it protects against mesangial expansion and fibronectin accumulation possibly by blunting podocyte VEGF increases. |
| 926 | 20375116 | Therefore, we generated two podocyte-specific GLUT1 transgenic mouse lines (driven by a podocin promoter) on a db/m C57BLKS background. |
| 927 | 20375116 | Levels of nephrin, neph1, CD2AP, podocin, and GLUT4 were not significantly different in transgenic compared with wild-type mice. |
| 928 | 20375116 | Taken together, increased podocyte GLUT1 expression in diabetic mice does not contribute to early diabetic nephropathy; surprisingly, it protects against mesangial expansion and fibronectin accumulation possibly by blunting podocyte VEGF increases. |
| 929 | 20457601 | CIN85/RukL is a novel binding partner of nephrin and podocin and mediates slit diaphragm turnover in podocytes. |
| 930 | 20457601 | Podocyte damage is the basis of many glomerular diseases with ultrastructural changes and decreased expression of components of the slit diaphragm such as nephrin and podocin. |
| 931 | 20457601 | In this manuscript we examined a mechanism of nephrin endocytosis via CIN85/Ruk(L)-mediated ubiquitination. |
| 932 | 20457601 | We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes. |
| 933 | 20457601 | In cultured murine podocytes CD2AP deficiency leads to an early ubiquitination of nephrin and podocin after stimulation with fibroblast growth factor-4. |
| 934 | 20457601 | Binding assays with different CIN85/Ruk isoforms and mutants showed that nephrin and podocin are binding to the coiled-coil domain of CIN85/Ruk(L). |
| 935 | 20457601 | We found that in the presence of CIN85/Ruk(L), which is involved in down-regulation of receptor-tyrosine kinases, nephrin is internalized after stimulation with fibroblast growth factor-4. |
| 936 | 20457601 | Interestingly, coexpression of CIN85/Ruk(L) with CD2AP led to a decreased binding of CIN85/Ruk(L) to nephrin and podocin, which indicates a functional competition between CD2AP and CIN85/Ruk(L). |
| 937 | 20457601 | CIN85/RukL is a novel binding partner of nephrin and podocin and mediates slit diaphragm turnover in podocytes. |
| 938 | 20457601 | Podocyte damage is the basis of many glomerular diseases with ultrastructural changes and decreased expression of components of the slit diaphragm such as nephrin and podocin. |
| 939 | 20457601 | In this manuscript we examined a mechanism of nephrin endocytosis via CIN85/Ruk(L)-mediated ubiquitination. |
| 940 | 20457601 | We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes. |
| 941 | 20457601 | In cultured murine podocytes CD2AP deficiency leads to an early ubiquitination of nephrin and podocin after stimulation with fibroblast growth factor-4. |
| 942 | 20457601 | Binding assays with different CIN85/Ruk isoforms and mutants showed that nephrin and podocin are binding to the coiled-coil domain of CIN85/Ruk(L). |
| 943 | 20457601 | We found that in the presence of CIN85/Ruk(L), which is involved in down-regulation of receptor-tyrosine kinases, nephrin is internalized after stimulation with fibroblast growth factor-4. |
| 944 | 20457601 | Interestingly, coexpression of CIN85/Ruk(L) with CD2AP led to a decreased binding of CIN85/Ruk(L) to nephrin and podocin, which indicates a functional competition between CD2AP and CIN85/Ruk(L). |
| 945 | 20457601 | CIN85/RukL is a novel binding partner of nephrin and podocin and mediates slit diaphragm turnover in podocytes. |
| 946 | 20457601 | Podocyte damage is the basis of many glomerular diseases with ultrastructural changes and decreased expression of components of the slit diaphragm such as nephrin and podocin. |
| 947 | 20457601 | In this manuscript we examined a mechanism of nephrin endocytosis via CIN85/Ruk(L)-mediated ubiquitination. |
| 948 | 20457601 | We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes. |
| 949 | 20457601 | In cultured murine podocytes CD2AP deficiency leads to an early ubiquitination of nephrin and podocin after stimulation with fibroblast growth factor-4. |
| 950 | 20457601 | Binding assays with different CIN85/Ruk isoforms and mutants showed that nephrin and podocin are binding to the coiled-coil domain of CIN85/Ruk(L). |
| 951 | 20457601 | We found that in the presence of CIN85/Ruk(L), which is involved in down-regulation of receptor-tyrosine kinases, nephrin is internalized after stimulation with fibroblast growth factor-4. |
| 952 | 20457601 | Interestingly, coexpression of CIN85/Ruk(L) with CD2AP led to a decreased binding of CIN85/Ruk(L) to nephrin and podocin, which indicates a functional competition between CD2AP and CIN85/Ruk(L). |
| 953 | 20457601 | CIN85/RukL is a novel binding partner of nephrin and podocin and mediates slit diaphragm turnover in podocytes. |
| 954 | 20457601 | Podocyte damage is the basis of many glomerular diseases with ultrastructural changes and decreased expression of components of the slit diaphragm such as nephrin and podocin. |
| 955 | 20457601 | In this manuscript we examined a mechanism of nephrin endocytosis via CIN85/Ruk(L)-mediated ubiquitination. |
| 956 | 20457601 | We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes. |
| 957 | 20457601 | In cultured murine podocytes CD2AP deficiency leads to an early ubiquitination of nephrin and podocin after stimulation with fibroblast growth factor-4. |
| 958 | 20457601 | Binding assays with different CIN85/Ruk isoforms and mutants showed that nephrin and podocin are binding to the coiled-coil domain of CIN85/Ruk(L). |
| 959 | 20457601 | We found that in the presence of CIN85/Ruk(L), which is involved in down-regulation of receptor-tyrosine kinases, nephrin is internalized after stimulation with fibroblast growth factor-4. |
| 960 | 20457601 | Interestingly, coexpression of CIN85/Ruk(L) with CD2AP led to a decreased binding of CIN85/Ruk(L) to nephrin and podocin, which indicates a functional competition between CD2AP and CIN85/Ruk(L). |
| 961 | 20457601 | CIN85/RukL is a novel binding partner of nephrin and podocin and mediates slit diaphragm turnover in podocytes. |
| 962 | 20457601 | Podocyte damage is the basis of many glomerular diseases with ultrastructural changes and decreased expression of components of the slit diaphragm such as nephrin and podocin. |
| 963 | 20457601 | In this manuscript we examined a mechanism of nephrin endocytosis via CIN85/Ruk(L)-mediated ubiquitination. |
| 964 | 20457601 | We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes. |
| 965 | 20457601 | In cultured murine podocytes CD2AP deficiency leads to an early ubiquitination of nephrin and podocin after stimulation with fibroblast growth factor-4. |
| 966 | 20457601 | Binding assays with different CIN85/Ruk isoforms and mutants showed that nephrin and podocin are binding to the coiled-coil domain of CIN85/Ruk(L). |
| 967 | 20457601 | We found that in the presence of CIN85/Ruk(L), which is involved in down-regulation of receptor-tyrosine kinases, nephrin is internalized after stimulation with fibroblast growth factor-4. |
| 968 | 20457601 | Interestingly, coexpression of CIN85/Ruk(L) with CD2AP led to a decreased binding of CIN85/Ruk(L) to nephrin and podocin, which indicates a functional competition between CD2AP and CIN85/Ruk(L). |
| 969 | 20522651 | Deletion of von Hippel-Lindau in glomerular podocytes results in glomerular basement membrane thickening, ectopic subepithelial deposition of collagen {alpha}1{alpha}2{alpha}1(IV), expression of neuroglobin, and proteinuria. |
| 970 | 20522651 | A component of the E3 ubiquitin ligase complex, von Hippel-Lindau (VHL) facilitates oxygen-dependent polyubiquitination and proteasomal degradation of HIFalpha subunits. |
| 971 | 20522651 | Hypothesizing that deletion of podocyte VHL would result in HIFalpha hyperstabilization, we crossed podocin promoter-Cre transgenic mice, which express Cre recombinase in podocytes beginning at the capillary loop stage of glomerular development, with floxed VHL mice. |
| 972 | 20634963 | CDKN1, DAG1, DDN, EHD3, MYH9, NES, NPHS1, NPHS2, PDPN, PLA2R1, PLCE1, PODXL, PTPRO, SYNPO, TCF21, TJP1, WT1). |
| 973 | 20634963 | This finding was further validated by assessing the expression of the axon guidance molecules neuritin (NRN1) and roundabout receptor ROBO1 and -2. |
| 974 | 20664558 | Several known slit diaphragm proteins were found, such as podocin and nephrin, confirming the validity of the purification scheme. |
| 975 | 20664558 | CLIC5 colocalized and associated with the ezrin/radixin/moesin complex and with podocalyxin in podocytes in vivo. |
| 976 | 20664558 | The ezrin/radixin/moesin complex and podocalyxin were significantly decreased in podocytes from CLIC5(-/-) mice. |
| 977 | 21030600 | Compared with vehicle-treated controls, paricalcitol preserved expression of nephrin, podocin, and WT1; prevented proteinuria; and reduced glomerulosclerotic lesions induced by ADR. |
| 978 | 21030600 | Selective suppression of renal Wnt4, Wnt7a, Wnt7b, and Wnt10a expression after ADR accompanied these renoprotective effects of paricalcitol. |
| 979 | 21030600 | In vitro, paricalcitol induced a physical interaction between the vitamin D receptor and β-catenin in podocytes, which led to suppression of β-catenin-mediated gene transcription. |
| 980 | 21071976 | Key genes that have been identified from the study of inherited NS include those encoding nephrin, podocin, TRPC6 and α-actinin-4, and more remain to be found. |
| 981 | 21151138 | Podocyte-specific transgenic overexpression of Angptl4 (NPHS2-Angptl4) in rats induced nephrotic-range, and selective, proteinuria (over 500-fold increase in albuminuria), loss of glomerular basement membrane (GBM) charge and foot process effacement, whereas transgenic expression specifically in the adipose tissue (aP2-Angptl4) resulted in increased circulating Angptl4, but no proteinuria. |
| 982 | 21289599 | Urinary albumin excretion increased in vehicle-treated diabetic rats (single injection of streptozotocin), compared with controls, and was associated with tubule injury and increased urinary tumor necrosis factor-α (TNF-α) at 9 weeks. |
| 983 | 21289599 | Further, both agonists restored WT-1 staining along with podocin and nephrin mRNA expression, suggesting podocyte protection. |
| 984 | 21329637 | Mutations in the MYH9 gene, encoding non-muscle myosin heavy chain IIA (NMMHC-IIA) have been identified in patients with MHA and other MYH9-related diseases. |
| 985 | 21329637 | Moreover, the expression of nephrin and podocin, slit diagram protein, was normal. |
| 986 | 21359962 | Nephrin and podocin expression levels were measured by real-time RT-PCR and Western blot. |
| 987 | 21359962 | The podocytes were treated by adriamycin in the presence or absence of HQH and nephrin and podocin expression and TNF-α and IL-1β synthesis and secretion were determined by real-time RT-PCR, immunoblotting, and ELISA, respectively. |
| 988 | 21359962 | Adriamycin significantly reduced nephrin and podocin expression, which was significantly restored by the treatment of HQH. |
| 989 | 21359962 | Nephrin and podocin expression levels were measured by real-time RT-PCR and Western blot. |
| 990 | 21359962 | The podocytes were treated by adriamycin in the presence or absence of HQH and nephrin and podocin expression and TNF-α and IL-1β synthesis and secretion were determined by real-time RT-PCR, immunoblotting, and ELISA, respectively. |
| 991 | 21359962 | Adriamycin significantly reduced nephrin and podocin expression, which was significantly restored by the treatment of HQH. |
| 992 | 21359962 | Nephrin and podocin expression levels were measured by real-time RT-PCR and Western blot. |
| 993 | 21359962 | The podocytes were treated by adriamycin in the presence or absence of HQH and nephrin and podocin expression and TNF-α and IL-1β synthesis and secretion were determined by real-time RT-PCR, immunoblotting, and ELISA, respectively. |
| 994 | 21359962 | Adriamycin significantly reduced nephrin and podocin expression, which was significantly restored by the treatment of HQH. |
| 995 | 21380797 | Plasma from a case of recurrent idiopathic FSGS perturbs non-muscle myosin IIA (MYH9 protein) in human podocytes. |
| 996 | 21380797 | The MYH9 gene encodes a non-muscle myosin IIA heavy chain (NMMHC-IIA) expressed in podocytes. |
| 997 | 21380797 | We demonstrate in vitro that plasmapheresis effluent from our patient rapidly decreased cultured podocyte levels of the phosphorylated myosin light chain (MLC) that mediates NMMHC-IIA binding to actin and induced dispersion of NMMHC-IIA from its usual position along actin stress fibers. |
| 998 | 21380797 | FSGS plasma also caused dispersion of slit diaphragm proteins (nephrin and podocin) and vinculin-positive focal adhesion complexes. |
| 999 | 21388638 | Expression of nephrin, podocin, α-actinin-4 and α3-integrin in canine renal glomeruli. |
| 1000 | 21388638 | The aim of this study was to investigate the expression and localization of nephrin, podocin, α-actinin-4 and α3-integrin in canine renal glomeruli. |
| 1001 | 21388638 | Expression of nephrin, podocin, α-actinin-4 and α3-integrin in canine renal glomeruli. |
| 1002 | 21388638 | The aim of this study was to investigate the expression and localization of nephrin, podocin, α-actinin-4 and α3-integrin in canine renal glomeruli. |
| 1003 | 21412216 | To test for a role of the bradykinin B1 receptor in podocyte injury, we pharmacologically modulated its activity at different time points in an adriamycin-induced mouse model of FSGS. |
| 1004 | 21412216 | Early treatment with a B1 antagonist reduced albuminuria and glomerulosclerosis, and inhibited the adriamycin-induced downregulation of podocin, nephrin, and α-actinin-4 expression. |
| 1005 | 21412216 | Thus, we propose that kinin has a crucial role in the pathogenesis of FSGS operating through bradykinin B1 receptor signaling. |
| 1006 | 21451433 | In vitro experiments used primary cultured podocytes harvested from mice carrying podocin-rtTA and TRE-hVEGF transgenes, in which hVEGF can be induced selectively. |
| 1007 | 21451433 | Induction of VEGF in PAN-exposed podocytes resulted in preservation of intrinsic VEGF, α-actinin-4 and synaptopodin, antiapoptotic marker Bcl-xL/Bax, as well as attenuation in apoptotic marker cleaved/total caspase-3. |
| 1008 | 21451433 | Furthermore, PAN-induced up-regulation of desmin, down-regulation of synaptopodin and nephrin, and disruption of glomerular morphology were significantly attenuated in VEGF-induced transgenic mice. |
| 1009 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1010 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1011 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1012 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1013 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1014 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1015 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1016 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1017 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1018 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1019 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1020 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1021 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1022 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1023 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1024 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1025 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1026 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1027 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1028 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1029 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1030 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1031 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1032 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1033 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1034 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1035 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1036 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1037 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1038 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1039 | 21478284 | Podocyte main slit diaphragm proteins, nephrin and podocin, are affected at early stages of lupus nephritis and correlate with disease histology. |
| 1040 | 21478284 | A putative disruption of the slit diaphragm and its main protein components, nephrin and podocin, may be implicated in the pathogenesis of lupus nephritis (LN). |
| 1041 | 21478284 | We studied the glomerular protein expression of nephrin and podocin in NZB/W LN mice by Western blot and immunofluorescence; mRNA levels were measured by real-time PCR. |
| 1042 | 21478284 | Glomerular protein expression of nephrin and podocin were significantly reduced in NZB/W LN, starting from the earlier stages (mild mesangial LN) and becoming pronounced at advanced histological forms (focal and diffuse proliferative LN). |
| 1043 | 21478284 | Nephrin and podocin mRNA levels were substantially decreased in diffuse proliferative disease. |
| 1044 | 21478284 | The main slit diaphragm proteins, nephrin and podocin, are affected from the earlier stages of LN and their expression correlates with disease histology. |
| 1045 | 21499232 | A GenBank analysis of the human podocin (NPHS2) gene resulted in the possible existence of a new splice variant of podocin in the kidney, missing the in-frame of exon 5, encoding the prohibitin homology domain. |
| 1046 | 21565142 | [Effects of Chinese herbal medicine Huaiqihuang Granule on nephrin and podocin expressions in renal tissues of rats with adriamycin-induced nephrosis]. |
| 1047 | 21632959 | In all lines, the quantities of NEPH1 and podocin proteins and NEPH1 and SYNPO mRNAs were comparable to glomeruli, while synaptopodin and nephrin proteins and NPHS1 and NPHS2 mRNAs were <5% of glomerular levels. |
| 1048 | 21653636 | Western blot and immunofluorescence analysis showed that podocyte markers (nephrin, CD2AP, podocin, Wilms' tumor-1) and an endothelial-specific molecule (VE-cadherin) were not detectable in this cell line, whereas markers characteristic of mesangial cells (α-SMA, fibronectin, and PDGFβ-R) were strongly expressed. |
| 1049 | 21694920 | Insulin resistance from excess fatty acids is exacerbated by decreased secretion of high molecular weight adiponectin from adipose cells in the obese state. |
| 1050 | 21694920 | Adiponectin potentiates insulin in its post-receptor signaling resulting in glucose oxidation in mitochondria. |
| 1051 | 21694920 | The architecture of the podocyte involves nephrin and podocin, proteins that cooperate to keep slit pores between foot processes competent to retain albumin. |
| 1052 | 21694920 | Insulin and adiponectin are necessary for high-energy phosphate generation. |
| 1053 | 21694920 | Fatty acid accumulation and resistin inhibit insulin and adiponectin. |
| 1054 | 21694920 | Study of cytokines produced by adipose tissue (adiponectin and leptin) and macrophages (resistin) has led to a better understanding of the relationship between weight and hypertension. |
| 1055 | 21719786 | Moreover, hCD25-negative podocytes, which were immune to the initial toxin injury, developed injury as early as 4 d after LMB2 injection, evidenced by foot process effacement, upregulation of desmin, and downregulation of nephrin, podocin, and podocalyxin. |
| 1056 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 1057 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 1058 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 1059 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 1060 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 1061 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 1062 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 1063 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 1064 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 1065 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 1066 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 1067 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 1068 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 1069 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 1070 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 1071 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 1072 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 1073 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 1074 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 1075 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 1076 | 21866094 | Induction of progressive glomerulonephritis by podocyte-specific overexpression of platelet-derived growth factor-D. |
| 1077 | 21866094 | Platelet-derived growth factor-D (PDGF-D), normally expressed in podocytes, mediates mesangial cell proliferation in vivo. |
| 1078 | 21866094 | Renal mRNA expression of podocin and nephrin, as well as the number of glomerular WT-1-positive cells, were significantly reduced in hemizygous compared to wild-type mice, indicating loss and/or dedifferentation of podocytes. |
| 1079 | 21866094 | PDGF-A, -B, and both PDGF receptor chain mRNAs, fibronectin, type IV collagen, RANTES, MCP-1, and CCR-2 mRNAs were all increased in the renal cortex of PDGF-D transgenic mice. |
| 1080 | 21953121 | For example, Alport syndrome develops from mutated type IV collagen that fosters the digestion of glomerular basement membranes and podocyte loss, followed by progressive glomerulosclerosis, ie Alport nephropathy. |
| 1081 | 21953121 | Etanercept treatment specifically reduced the numbers of apoptotic podocytes, increased total podocyte counts, and increased the renal mRNA expression of nephrin and podocin without affecting markers of renal inflammation. |
| 1082 | 22052048 | The podocytes of these mice exhibited foot process effacement with reduced and altered localization of the slit-diaphragm proteins nephrin and podocin. |
| 1083 | 22056625 | The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, simultaneously regulates Rac1 and Cdc42, which destabilize the podocyte actin cytoskeleton during early DN. |
| 1084 | 22056625 | In this study, in order to evaluate the reno-protective effects of wortmannin in early DN by regulating Rac1 and Cdc42, streptozotocin (STZ)-induced proteinuric renal disease (SPRD) rats were treated with wortmannin. |
| 1085 | 22056625 | Changes in the expression level of nephrin, podocin and Rac1/Cdc42, which is related to actin cytoskeleton in podocytes, by wortmannin administration were confirmed by Western blotting. |
| 1086 | 22056625 | The expression levels of nephrin (79.66 ± 0.02), podocin (87.81 ± 0.03) and Rac1/Cdc42 (86.12 ± 0.02) in the wortmannin group were higher than the expression levels of nephrin (55.32 ± 0.03), podocin (53.40 ± 0.06) and Rac1/Cdc42 (54.05 ± 0.04) in the SPRD group. |
| 1087 | 22056625 | In addition, expression and localization of nephrin, podocin and desmin were confirmed by immunofluorescence. |
| 1088 | 22056625 | The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, simultaneously regulates Rac1 and Cdc42, which destabilize the podocyte actin cytoskeleton during early DN. |
| 1089 | 22056625 | In this study, in order to evaluate the reno-protective effects of wortmannin in early DN by regulating Rac1 and Cdc42, streptozotocin (STZ)-induced proteinuric renal disease (SPRD) rats were treated with wortmannin. |
| 1090 | 22056625 | Changes in the expression level of nephrin, podocin and Rac1/Cdc42, which is related to actin cytoskeleton in podocytes, by wortmannin administration were confirmed by Western blotting. |
| 1091 | 22056625 | The expression levels of nephrin (79.66 ± 0.02), podocin (87.81 ± 0.03) and Rac1/Cdc42 (86.12 ± 0.02) in the wortmannin group were higher than the expression levels of nephrin (55.32 ± 0.03), podocin (53.40 ± 0.06) and Rac1/Cdc42 (54.05 ± 0.04) in the SPRD group. |
| 1092 | 22056625 | In addition, expression and localization of nephrin, podocin and desmin were confirmed by immunofluorescence. |
| 1093 | 22056625 | The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, simultaneously regulates Rac1 and Cdc42, which destabilize the podocyte actin cytoskeleton during early DN. |
| 1094 | 22056625 | In this study, in order to evaluate the reno-protective effects of wortmannin in early DN by regulating Rac1 and Cdc42, streptozotocin (STZ)-induced proteinuric renal disease (SPRD) rats were treated with wortmannin. |
| 1095 | 22056625 | Changes in the expression level of nephrin, podocin and Rac1/Cdc42, which is related to actin cytoskeleton in podocytes, by wortmannin administration were confirmed by Western blotting. |
| 1096 | 22056625 | The expression levels of nephrin (79.66 ± 0.02), podocin (87.81 ± 0.03) and Rac1/Cdc42 (86.12 ± 0.02) in the wortmannin group were higher than the expression levels of nephrin (55.32 ± 0.03), podocin (53.40 ± 0.06) and Rac1/Cdc42 (54.05 ± 0.04) in the SPRD group. |
| 1097 | 22056625 | In addition, expression and localization of nephrin, podocin and desmin were confirmed by immunofluorescence. |
| 1098 | 22137726 | The mechanisms underlying glomerular disease are very variable and include infiltration of inflammatory cells, proliferation of glomerular cells, and malfunction of podocyte-associated molecules such as nephrin or podocin. |
| 1099 | 22137726 | The multiligand receptors megalin and cubilin are responsible for the constitutive uptake in this mechanism. |
| 1100 | 22137726 | TGF-β, which may be induced by albumin exposure, may also act in a feedback mechanism increasing albumin filtration and at the same time inhibiting megalin- and cubilin-mediated albumin endocytosis, leading to increased albuminuria. |
| 1101 | 22207085 | Bufalin alleviated the removal of podocyte foot processes and attenuated the changes in nephrin, podocin and integrin-linked kinase (ILK) stainings in the glomerulus of the ADR rats. |
| 1102 | 22207085 | Bufalin notably decreased the expression of nephrin and ILK but inhibited the down-regulation of podocin in protein levels on the renal cortex of the ADR rats. |
| 1103 | 22207085 | Additionally, bufalin inhibited the up-regulation of podocin and ILK in mRNA levels but did not affect nephrin mRNA levels. |
| 1104 | 22207085 | Bufalin alleviated the removal of podocyte foot processes and attenuated the changes in nephrin, podocin and integrin-linked kinase (ILK) stainings in the glomerulus of the ADR rats. |
| 1105 | 22207085 | Bufalin notably decreased the expression of nephrin and ILK but inhibited the down-regulation of podocin in protein levels on the renal cortex of the ADR rats. |
| 1106 | 22207085 | Additionally, bufalin inhibited the up-regulation of podocin and ILK in mRNA levels but did not affect nephrin mRNA levels. |
| 1107 | 22207085 | Bufalin alleviated the removal of podocyte foot processes and attenuated the changes in nephrin, podocin and integrin-linked kinase (ILK) stainings in the glomerulus of the ADR rats. |
| 1108 | 22207085 | Bufalin notably decreased the expression of nephrin and ILK but inhibited the down-regulation of podocin in protein levels on the renal cortex of the ADR rats. |
| 1109 | 22207085 | Additionally, bufalin inhibited the up-regulation of podocin and ILK in mRNA levels but did not affect nephrin mRNA levels. |
| 1110 | 22249312 | QLα12(LacZ+/Cre+) mice showed no changes in podocyte number, apoptosis, proliferation or Rho/Src activation. |
| 1111 | 22249312 | Real-time PCR revealed no significant changes in Nphs1, Nphs2, Cd2ap or Trpc6 expression, but Col4a2 message was increased in younger and older mice, while Col4a5 was decreased in older mice. |
| 1112 | 22249312 | Confocal microscopy revealed disordered collagen IVα1/2 staining in older mice and loss of α5 without changes in other collagen IV subunits. |
| 1113 | 22249312 | Taken together, these studies suggest that Gα12 activation promotes glomerular injury without podocyte depletion through a novel mechanism regulating collagen (α)IV expression, and supports the notion that glomerular damage may accrue through persistent GPCR activation in podocytes. |
| 1114 | 22493483 | In comparison with known CREB target genes, we identified Krüppel-like factor 15 (KLF15), a kidney-enriched nuclear transcription factor, that has been previously shown to mediate cell differentiation. |
| 1115 | 22493483 | Also, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocytes. |
| 1116 | 22582804 | Urine and serum biochemical parameters, serum TNF-α and IL-1β levels, nephrin, podocin, α-actinin-4, and peroxisome proliferator-activated receptor-α (PPAR-α) protein expression, and renal ultrastructure were examined at day 28. |
| 1117 | 22582804 | Compared with those in control rats, nephrin, podocin, and PPAR-α protein expressions decreased in the glomeruli of DOX-treated rats, and this effect was significantly attenuated by 1. |
| 1118 | 22582804 | SN ameliorates DOX-induced nephrotic syndrome in rats, resulting in a modulation of renal nephrin, podocin expression, and thereby protecting podocytes from injury. |
| 1119 | 22582804 | Urine and serum biochemical parameters, serum TNF-α and IL-1β levels, nephrin, podocin, α-actinin-4, and peroxisome proliferator-activated receptor-α (PPAR-α) protein expression, and renal ultrastructure were examined at day 28. |
| 1120 | 22582804 | Compared with those in control rats, nephrin, podocin, and PPAR-α protein expressions decreased in the glomeruli of DOX-treated rats, and this effect was significantly attenuated by 1. |
| 1121 | 22582804 | SN ameliorates DOX-induced nephrotic syndrome in rats, resulting in a modulation of renal nephrin, podocin expression, and thereby protecting podocytes from injury. |
| 1122 | 22582804 | Urine and serum biochemical parameters, serum TNF-α and IL-1β levels, nephrin, podocin, α-actinin-4, and peroxisome proliferator-activated receptor-α (PPAR-α) protein expression, and renal ultrastructure were examined at day 28. |
| 1123 | 22582804 | Compared with those in control rats, nephrin, podocin, and PPAR-α protein expressions decreased in the glomeruli of DOX-treated rats, and this effect was significantly attenuated by 1. |
| 1124 | 22582804 | SN ameliorates DOX-induced nephrotic syndrome in rats, resulting in a modulation of renal nephrin, podocin expression, and thereby protecting podocytes from injury. |
| 1125 | 22662192 | In podocytes, IQGAP1 is associated with nephrin in the glomerular slit diaphragm (SD) complex, but its role remains ill-defined. |
| 1126 | 22662192 | IC, IP, and IsPL experiments showed colocalizations and/or interactions between IQGAP1 and SD proteins (nephrin, MAGI-1, CD2AP, NCK 1/2, podocin), podocalyxin, and cytoskeletal proteins (α-actinin-4). |
| 1127 | 22693670 | The close relationships of slit diaphragm (SD) molecules such as nephrin, podocin, CD2-associated protein (CD2AP), a-actinin-4, transient receptor potential cation channel 6 (TRPC6), Densin and membrane-associated guanylate kinase inverted 1 (MAGI-1), α3β1 integrin, WT1, phospholipase C epsilon-1 (PLCE1), Lmx1b, and MYH9, and mitochondrial disorders and circulating factors in the pathogenesis of glomerular proteinuria were also gradually discovered. |
| 1128 | 22773827 | We generated transgenic Fischer 344 rats that express a dominant negative AA-4E-BP1 transgene driven by the podocin promoter; a member of the mammalian target of rapamycin complex 1 (mTORC1) pathway, 4E-BP1 modulates cap-dependent translation, which is a key determinant of a cell's hypertrophic response to nutrients and growth factors. |
| 1129 | 22782578 | Key genes that have been identified from the study of inherited nephrotic syndromes include those encoding nephrin, podocin, TRPC6 (transient receptor potential canonical channel-6) and α-actinin-4, and more remain to be found. |
| 1130 | 22808199 | Tet-O-siVEGF:podocin-rtTA mice express VEGF shRNA in podocytes in a doxycycline-regulated manner, decreasing VEGF-A mRNA and VEGF-A protein levels in isolated glomeruli to ~20% of non-induced controls and urine VEGF-A to ~30% of control values a week after doxycycline induction. |
| 1131 | 22808199 | VEGF receptor-2 (VEGFR2) interacts with beta(3) integrin and neuropilin-1 in the kidney in vivo and in VEGF(KD) podocytes. |
| 1132 | 22808199 | Collectively, these studies indicate that podocyte VEGF-A regulates alpha(V)beta(3) integrin signaling in the glomerulus, and that podocyte VEGF knockdown disrupts alpha(V)beta(3) integrin activity via decreased VEGFR2 signaling, thereby damaging the three layers of the glomerular filtration barrier, causing proteinuria and acute renal failure. |
| 1133 | 22848482 | In diabetic mice, orally administration of genipin postponed the progression of DN, as demonstrated by ameliorating body weight loss and urine albumin leakage, attenuating glomerular basement membrane thickness, restoring the podocyte expression of podocin and WT1 in diabetic mice. |
| 1134 | 22848482 | Meanwhile, through inhibiting the up-regulation of UCP2, genipin restores podocin and WT1 expression in cultured podocytes and attenuates glucose-induced albumin leakage through podocytes monolayer. |
| 1135 | 22848482 | In diabetic mice, orally administration of genipin postponed the progression of DN, as demonstrated by ameliorating body weight loss and urine albumin leakage, attenuating glomerular basement membrane thickness, restoring the podocyte expression of podocin and WT1 in diabetic mice. |
| 1136 | 22848482 | Meanwhile, through inhibiting the up-regulation of UCP2, genipin restores podocin and WT1 expression in cultured podocytes and attenuates glucose-induced albumin leakage through podocytes monolayer. |
| 1137 | 23024785 | The present study generated and characterized the mice lacking cystathionine β-synthase (Cbs) and Asm mouse gene by cross breeding Cbs(+/-) and Asm(+/-) mice. |
| 1138 | 23024785 | Given that the homozygotes of Cbs(-/-/)Asm(-/-) mice could not survive for 3 weeks. |
| 1139 | 23024785 | Cbs(+/-/)Asm(+/+), Cbs(+/-/)Asm(+/-) and Cbs(+/-/)Asm(-/-) as well as their Cbs wild type littermates were used to study the role of Asm(-/-) under a background of Cbs(+/-) with hHcys. |
| 1140 | 23024785 | HPLC analysis revealed that plasma Hcys level was significantly elevated in Cbs heterozygous (Cbs(+/-)) mice with different copies of Asm gene compared to Cbs(+/+) mice with different Asm gene copies. |
| 1141 | 23024785 | Cbs(+/-/)Asm(+/+) mice had significantly increased renal Asm activity, ceramide production and O(2.)(-) level compared to Cbs(+/+)/Asm(+/+), while Cbs(+/-/)Asm(-/-) mice showed significantly reduced renal Asm activity, ceramide production and O(2.)(-) level due to increased plasma Hcys levels. |
| 1142 | 23024785 | Confocal microscopy demonstrated that colocalization of podocin with ceramide was much lower in Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice, which was accompanied by a reduced glomerular damage index, albuminuria and proteinuria in Cbs(+/-/)Asm(-/-) mice. |
| 1143 | 23024785 | Immunofluorescent analyses of the podocin, nephrin and desmin expression also illustrated less podocyte damages in the glomeruli from Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice. |
| 1144 | 23024785 | In in vitro studies of podocytes, hHcys-enhanced O(2.)(-) production, desmin expression, and ceramide production as well as decreases in VEGF level and podocin expression in podocytes were substantially attenuated by prior treatment with amitriptyline, an Asm inhibitor. |
| 1145 | 23024785 | The present study generated and characterized the mice lacking cystathionine β-synthase (Cbs) and Asm mouse gene by cross breeding Cbs(+/-) and Asm(+/-) mice. |
| 1146 | 23024785 | Given that the homozygotes of Cbs(-/-/)Asm(-/-) mice could not survive for 3 weeks. |
| 1147 | 23024785 | Cbs(+/-/)Asm(+/+), Cbs(+/-/)Asm(+/-) and Cbs(+/-/)Asm(-/-) as well as their Cbs wild type littermates were used to study the role of Asm(-/-) under a background of Cbs(+/-) with hHcys. |
| 1148 | 23024785 | HPLC analysis revealed that plasma Hcys level was significantly elevated in Cbs heterozygous (Cbs(+/-)) mice with different copies of Asm gene compared to Cbs(+/+) mice with different Asm gene copies. |
| 1149 | 23024785 | Cbs(+/-/)Asm(+/+) mice had significantly increased renal Asm activity, ceramide production and O(2.)(-) level compared to Cbs(+/+)/Asm(+/+), while Cbs(+/-/)Asm(-/-) mice showed significantly reduced renal Asm activity, ceramide production and O(2.)(-) level due to increased plasma Hcys levels. |
| 1150 | 23024785 | Confocal microscopy demonstrated that colocalization of podocin with ceramide was much lower in Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice, which was accompanied by a reduced glomerular damage index, albuminuria and proteinuria in Cbs(+/-/)Asm(-/-) mice. |
| 1151 | 23024785 | Immunofluorescent analyses of the podocin, nephrin and desmin expression also illustrated less podocyte damages in the glomeruli from Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice. |
| 1152 | 23024785 | In in vitro studies of podocytes, hHcys-enhanced O(2.)(-) production, desmin expression, and ceramide production as well as decreases in VEGF level and podocin expression in podocytes were substantially attenuated by prior treatment with amitriptyline, an Asm inhibitor. |
| 1153 | 23024785 | The present study generated and characterized the mice lacking cystathionine β-synthase (Cbs) and Asm mouse gene by cross breeding Cbs(+/-) and Asm(+/-) mice. |
| 1154 | 23024785 | Given that the homozygotes of Cbs(-/-/)Asm(-/-) mice could not survive for 3 weeks. |
| 1155 | 23024785 | Cbs(+/-/)Asm(+/+), Cbs(+/-/)Asm(+/-) and Cbs(+/-/)Asm(-/-) as well as their Cbs wild type littermates were used to study the role of Asm(-/-) under a background of Cbs(+/-) with hHcys. |
| 1156 | 23024785 | HPLC analysis revealed that plasma Hcys level was significantly elevated in Cbs heterozygous (Cbs(+/-)) mice with different copies of Asm gene compared to Cbs(+/+) mice with different Asm gene copies. |
| 1157 | 23024785 | Cbs(+/-/)Asm(+/+) mice had significantly increased renal Asm activity, ceramide production and O(2.)(-) level compared to Cbs(+/+)/Asm(+/+), while Cbs(+/-/)Asm(-/-) mice showed significantly reduced renal Asm activity, ceramide production and O(2.)(-) level due to increased plasma Hcys levels. |
| 1158 | 23024785 | Confocal microscopy demonstrated that colocalization of podocin with ceramide was much lower in Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice, which was accompanied by a reduced glomerular damage index, albuminuria and proteinuria in Cbs(+/-/)Asm(-/-) mice. |
| 1159 | 23024785 | Immunofluorescent analyses of the podocin, nephrin and desmin expression also illustrated less podocyte damages in the glomeruli from Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice. |
| 1160 | 23024785 | In in vitro studies of podocytes, hHcys-enhanced O(2.)(-) production, desmin expression, and ceramide production as well as decreases in VEGF level and podocin expression in podocytes were substantially attenuated by prior treatment with amitriptyline, an Asm inhibitor. |
| 1161 | 23029287 | Immunofluorescence staining indicated that the expression of nephrin and podocin were both decreased after exposure of GDF. |
| 1162 | 23029522 | Following 10 days of directed differentiation, iPS podocytes had an up-regulated expression of mRNA and protein localization for podocyte markers including synaptopodin, nephrin and Wilm's tumour protein (WT1), combined with a down-regulation of the stem cell marker OCT3/4. |
| 1163 | 23029522 | The transduction of iPS podocytes with fluorescent labeled-talin that were immunostained with podocin showed a cytoplasmic contractile response to angiotensin II (AII). |
| 1164 | 23090771 | Significantly elevated mRNA levels of nephrin, podocin, and vascular endothelial growth factor were detected in preeclamptic women compared with healthy pregnant and healthy nonpregnant controls. |
| 1165 | 23090771 | A positive correlation (ρ=0.82; P<0.0001) was observed between nephrin and vascular endothelial growth factor mRNA levels in preeclamptic women. |
| 1166 | 23223090 | The maximally effective dose of valsartan was determined to be 1000 mg/l, which reduced proteinuria by 80% and maximally reduced glomerular matrix expansion, fibronectin, collagen I and collagen III staining and glomerular mRNAs for TGFß1, PAI-1, FN and collagen I. |
| 1167 | 23223090 | Notably, valsartan given at this dose prevented podocyte dysfunction by preserving expression of podocin and nephrin and the counter-regulating molecule B7-1 that is involved in podocyte injury. |
| 1168 | 23296190 | In addition to these receptors, Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene 1 (RIG-I)-like helicases (RLHs), podocytes express the collateral proteins required to support intracellular signaling. |
| 1169 | 23296190 | The transcription factor interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-ĸB) are phosphorylated and translocate to the nucleus, and dsRNA increases synthesis of proteins driven by IRF3 (P54, P56 and P60) or NF-ĸB (interleukin 8 and A20). |
| 1170 | 23296190 | Furthermore, dsRNA suppresses podocyte cell migration, alters the expression of a panel of podocyte essential proteins (nephrin, podocin and CD2-associated protein or CD2AP) and changes transepithelial albumin flux. |
| 1171 | 23436459 | Active proteases in nephrotic plasma lead to a podocin-dependent phosphorylation of VASP in podocytes via protease activated receptor-1. |
| 1172 | 23436459 | By the use of siRNA technology, we show that proteases in the plasma signal predominantly via protease activated receptor-1 (PAR1) to VASP. |
| 1173 | 23437316 | Its gene product, the stomatin family member protein podocin represents a core component of the slit diaphragm, a unique structure that bridges the space between adjacent podocyte foot processes in the kidney glomerulus. |
| 1174 | 23466998 | Treatment of these transgenic zebrafish with metronidazole results in podocyte apoptosis, a loss of nephrin and podocin expression, foot process effacement, and a leaky glomerular filtration barrier. |
| 1175 | 23466998 | Following metronidazole washout, proliferating cells were detected in the glomeruli of recovering transgenic fish with a restoration of nitroreductase-GFP fluorescence, nephrin and podocin expression, a reestablishment of normal foot process architecture, and glomerular barrier function. |
| 1176 | 23466998 | Treatment of these transgenic zebrafish with metronidazole results in podocyte apoptosis, a loss of nephrin and podocin expression, foot process effacement, and a leaky glomerular filtration barrier. |
| 1177 | 23466998 | Following metronidazole washout, proliferating cells were detected in the glomeruli of recovering transgenic fish with a restoration of nitroreductase-GFP fluorescence, nephrin and podocin expression, a reestablishment of normal foot process architecture, and glomerular barrier function. |
| 1178 | 23529346 | Correspondingly, rmGH treatment also blocked hHcys-induced decrease in the expression of podocin, a podocyte slit diaphragm molecule, and inhibited the increases in the expression of desmin, a podocyte injury marker. |
| 1179 | 23529346 | It was also demonstrated that in hHcys the expression of epithelial markers, p-cadherin and ZO-1, decreased, while the expression of mesenchymal markers, antifibroblast-specific protein 1 (FSP-1) and α-SMA, increased in podocytes, which together suggest the activation of EMT in podocytes. |
| 1180 | 23529346 | Nicotinamide adenine dinucleotide phosphate oxidase (Nox)-dependent superoxide anion (O2 (.-)) and hypoxia-inducible factor-1α (HIF-1α) level in the hHcys mice cortex was markedly enhanced. |
| 1181 | 23547922 | These animal models include the reduction of renal mass by resecting 5/6 of the kidney, reduction of renal mass due to systemic diseases such as hypertension, hyperlipidemia or SLE, drug-induced FSGS using adriamycin, puromycin or streptozotocin, virus-induced FSGS, genetically-induced FSGS such as via Mpv-17 inactivation and α-actinin 4 and podocin knockouts, and a model for circulating permeability factors. |
| 1182 | 23552865 | Moreover, we found a reduction of specific markers such as Wilm's tumor-1, podocin, and synaptopodin in both experimental groups indicating a loss of podocytes. |
| 1183 | 23555556 | In both in vivo and in vitro studies, the expression of synaptopodin, a molecular marker for podocyte integrity, and the slit diaphragm constituting molecules (SDCM), such as nephrin, podocin, and CD2-associated protein (CD2AP), were decreased in morphine-treated podocytes. |
| 1184 | 23555556 | In addition, AKT, p38, and JNK pathways were involved in morphine-induced down regulation of SDCM in human podocytes. |
| 1185 | 23582971 | The aim of this study was to investigate the temporal relationship between the expression of five podocyte proteins (nephrin, podocin, synaptopodin, α-actinin-4 and α3-integrin) and the development of podocyte injuries, proteinuria and glomerulosclerosis in OM rats. |
| 1186 | 23676370 | We evaluated the effects of chronic treatment with tolvaptan on renal dysfunction, podocyte injury, inflammation, oxidative stress, Rho-kinase, epithelial-mesenchymal transition (EMT), and the extracellular signal-regulated protein kinase (ERK1/2) pathway in the renal cortex of Dahl salt-sensitive hypertensive (DS) rats with end-stage severe HF. |
| 1187 | 23676370 | Decreased expression of nephrin and podocin and increased desmin-positive area in failing rats were restored by tolvaptan. |
| 1188 | 23676370 | Upregulation of NAD(P)H oxidase p22(phox), p47(phox), and gp91(phox), EMT markers such as transforming growth factor-β1, vimentin, and fibronectin expression, and Rho-kinase and ERK1/2 phosphorylation in DS rats were significantly suppressed by tolvaptan. |
| 1189 | 23676370 | Tolvaptan administration resulted in significant inhibition of tumor necrosis factor-α and monocyte chemoattractant protein-1 expression, and nuclear factor-κB phosphorylation. |
| 1190 | 23676370 | We concluded that long-term tolvaptan therapy may improve renal dysfunction, glomerulosclerosis, podocyte injury, and inflammation associated with oxidative stress, as well as EMT, ERK, and the Rho-kinase pathway in the failing heart of DS rats. |
| 1191 | 23677246 | Divergent functions of the Rho GTPases Rac1 and Cdc42 in podocyte injury. |
| 1192 | 23677246 | The mammalian Rho GTPases Rac1 and Cdc42 are molecular switches that control many cellular processes, but are best known for their roles in the regulation of actin cytoskeleton dynamics. |
| 1193 | 23677246 | In addition, slit diaphragm proteins nephrin and podocin were redistributed, and cofilin was dephosphorylated. |
| 1194 | 23677246 | Thus, our study highlights the divergent roles of Rac1 and Cdc42 function in podocyte maintenance and injury. |
| 1195 | 23710468 | Compared to KK-a/a controls, 26-week-old KK-A (y) mice had elevated HbA1c, insulin, leptin, triglycerides, and cholesterol, and Unx further elevated these markers of metabolic dysregulation. |
| 1196 | 23710468 | Consistent with functional and histological evidence of increased injury, fibrotic (fibronectin 1, MMP9, and TGF β 1) and inflammatory (IL-6, CD68) genes were markedly upregulated in Unx KK-A (y) mice, while podocyte markers (nephrin and podocin) were significantly decreased. |
| 1197 | 23761667 | We detected the dynamic changes of urinary protein, urinary F2-isoprostane and renal malondialdehyde levels, kidney ultrastructure morphology, mitochondrial DNA (mtDNA) copy number, mitochondrial membrane potential (ΔΨm), and nephrin and podocin expressions in Aldo-infused mice. |
| 1198 | 23761667 | In cultured podocytes, Aldo or hydrogen peroxide (H2O2) induced MtD after 2-8 h of treatment, whereas the podocyte damage, as shown by decreased nephrin and podocin expressions, occurred later after 12 h of treatment. |
| 1199 | 23761667 | We detected the dynamic changes of urinary protein, urinary F2-isoprostane and renal malondialdehyde levels, kidney ultrastructure morphology, mitochondrial DNA (mtDNA) copy number, mitochondrial membrane potential (ΔΨm), and nephrin and podocin expressions in Aldo-infused mice. |
| 1200 | 23761667 | In cultured podocytes, Aldo or hydrogen peroxide (H2O2) induced MtD after 2-8 h of treatment, whereas the podocyte damage, as shown by decreased nephrin and podocin expressions, occurred later after 12 h of treatment. |
| 1201 | 23769837 | A subset of cells lining Bowman's capsule activated expression of the glomerular parietal epithelial cell markers paired box protein PAX2 and claudin-1. |
| 1202 | 23769837 | A subset of labeled cells within the glomerular tuft expressed the podocyte markers Wilms tumor protein 1, nephrin, podocin, and synaptopodin. |
| 1203 | 23799145 | Angiotensin II receptor blocker attenuates intrarenal renin-angiotensin-system and podocyte injury in rats with myocardial infarction. |
| 1204 | 23799145 | The present study aimed to test the hypothesis that angiotensin II type 1 receptor blockers (ARBs) provides renoprotective effects after MI by preventing augmented intrarenal renin-angiotensin-system (RAS)-induced podocyte injury. |
| 1205 | 23799145 | The current study revealed that MI-induced glomerular podocyte injury was identified by increased immunostaining for desmin and p16(ink4a), decreased immunostaining for Wilms' tumor-1 and podocin mRNA expression, and an induced increase of blood cystatin C at both 3 and 9 weeks. |
| 1206 | 23799145 | These changes were associated with increased intrarenal angiotensin II levels and enhanced expressions of angiotensinogen mRNA and angiotensin II receptor mRNA and protein. |
| 1207 | 23799145 | These changes were also associated with decreased levels of insulin-like growth factor (IGF-1) and decreased expressions of IGF-1 receptor (IGF-1R) protein and mRNA and phosphorylated(p)-Akt protein at 9 weeks, as well as increased expressions of 8-hydroxy-2'-deoxyguanosine at both time points. |
| 1208 | 23799145 | Treatment with losartan significantly attenuated desmin- and p16(ink4a)-positive podocytes, restored podocin mRNA expression, and decreased blood cystatin C levels. |
| 1209 | 23799145 | Losartan also prevented RAS activation and oxidative stress and restored the IGF-1/IGF-1R/Akt pathway. |
| 1210 | 23799145 | In conclusion, ARBs prevent the progression of renal impairment after MI via podocyte protection, partially by inhibiting the activation of the local RAS with subsequent enhanced oxidative stress and an inhibited IGF-1/IGF-1R/Akt pathway. |
| 1211 | 23799145 | Angiotensin II receptor blocker attenuates intrarenal renin-angiotensin-system and podocyte injury in rats with myocardial infarction. |
| 1212 | 23799145 | The present study aimed to test the hypothesis that angiotensin II type 1 receptor blockers (ARBs) provides renoprotective effects after MI by preventing augmented intrarenal renin-angiotensin-system (RAS)-induced podocyte injury. |
| 1213 | 23799145 | The current study revealed that MI-induced glomerular podocyte injury was identified by increased immunostaining for desmin and p16(ink4a), decreased immunostaining for Wilms' tumor-1 and podocin mRNA expression, and an induced increase of blood cystatin C at both 3 and 9 weeks. |
| 1214 | 23799145 | These changes were associated with increased intrarenal angiotensin II levels and enhanced expressions of angiotensinogen mRNA and angiotensin II receptor mRNA and protein. |
| 1215 | 23799145 | These changes were also associated with decreased levels of insulin-like growth factor (IGF-1) and decreased expressions of IGF-1 receptor (IGF-1R) protein and mRNA and phosphorylated(p)-Akt protein at 9 weeks, as well as increased expressions of 8-hydroxy-2'-deoxyguanosine at both time points. |
| 1216 | 23799145 | Treatment with losartan significantly attenuated desmin- and p16(ink4a)-positive podocytes, restored podocin mRNA expression, and decreased blood cystatin C levels. |
| 1217 | 23799145 | Losartan also prevented RAS activation and oxidative stress and restored the IGF-1/IGF-1R/Akt pathway. |
| 1218 | 23799145 | In conclusion, ARBs prevent the progression of renal impairment after MI via podocyte protection, partially by inhibiting the activation of the local RAS with subsequent enhanced oxidative stress and an inhibited IGF-1/IGF-1R/Akt pathway. |
| 1219 | 23874454 | We previously reported that podocyte-specific deletion of Myh9 (conventional myosin heavy chain 2A) in C57BL/6 mice does not cause spontaneous kidney disease but instead results in a predisposition to glomerulosclerosis in response to a second model of glomerular injury. |
| 1220 | 23874454 | In order to elucidate the cause of this strain dependent effect Podocin::Cre and Myh9(flox) alleles were backcrossed to mouse strain FVB/N, which is highly susceptible to glomerulosclerosis, with the aim of intercrossing susceptible FVB/N and resistant C57BL/6 mice in subsequent congenic analyses. |
| 1221 | 23948707 | NOX2 interacts with podocyte TRPC6 channels and contributes to their activation by diacylglycerol: essential role of podocin in formation of this complex. |
| 1222 | 23948707 | TRPC6 channels are typically activated by diacylglycerol (DAG) during PLC-dependent transduction cascades. |
| 1223 | 23948707 | We previously showed that podocin is required for DAG analogs to produce robust activation of TRPC6 channels in podocytes. |
| 1224 | 23948707 | Here we show that endogenous TRPC6 channels in immortalized podocytes reciprocally coimmunoprecipitate with the catalytic subunit of the NADPH oxidase NOX2 (gp91(phox)). |
| 1225 | 23948707 | The NOX2-TRPC6 interaction was not detected in cells stably expressing a short hairpin RNA targeting podocin, although NOX2 and TRPC6 were present at normal levels. |
| 1226 | 23948707 | OAG also increased steady-state surface expression of the NOX2 regulatory subunit p47(phox). |
| 1227 | 23948707 | In whole cell recordings, TRPC6 activation by OAG was reduced in podocytes pretreated with the NOX2 inhibitor apocynin, by the pan-NOX inhibitor diphenylene iodonium, and by tempol, a ROS quencher. |
| 1228 | 23948707 | These data suggest that active NOX2 assembles with TRPC6 at podocin-organized sterol-rich raft domains and becomes catalytically active in response to DAG. |
| 1229 | 23948707 | NOX2 interacts with podocyte TRPC6 channels and contributes to their activation by diacylglycerol: essential role of podocin in formation of this complex. |
| 1230 | 23948707 | TRPC6 channels are typically activated by diacylglycerol (DAG) during PLC-dependent transduction cascades. |
| 1231 | 23948707 | We previously showed that podocin is required for DAG analogs to produce robust activation of TRPC6 channels in podocytes. |
| 1232 | 23948707 | Here we show that endogenous TRPC6 channels in immortalized podocytes reciprocally coimmunoprecipitate with the catalytic subunit of the NADPH oxidase NOX2 (gp91(phox)). |
| 1233 | 23948707 | The NOX2-TRPC6 interaction was not detected in cells stably expressing a short hairpin RNA targeting podocin, although NOX2 and TRPC6 were present at normal levels. |
| 1234 | 23948707 | OAG also increased steady-state surface expression of the NOX2 regulatory subunit p47(phox). |
| 1235 | 23948707 | In whole cell recordings, TRPC6 activation by OAG was reduced in podocytes pretreated with the NOX2 inhibitor apocynin, by the pan-NOX inhibitor diphenylene iodonium, and by tempol, a ROS quencher. |
| 1236 | 23948707 | These data suggest that active NOX2 assembles with TRPC6 at podocin-organized sterol-rich raft domains and becomes catalytically active in response to DAG. |
| 1237 | 23948707 | NOX2 interacts with podocyte TRPC6 channels and contributes to their activation by diacylglycerol: essential role of podocin in formation of this complex. |
| 1238 | 23948707 | TRPC6 channels are typically activated by diacylglycerol (DAG) during PLC-dependent transduction cascades. |
| 1239 | 23948707 | We previously showed that podocin is required for DAG analogs to produce robust activation of TRPC6 channels in podocytes. |
| 1240 | 23948707 | Here we show that endogenous TRPC6 channels in immortalized podocytes reciprocally coimmunoprecipitate with the catalytic subunit of the NADPH oxidase NOX2 (gp91(phox)). |
| 1241 | 23948707 | The NOX2-TRPC6 interaction was not detected in cells stably expressing a short hairpin RNA targeting podocin, although NOX2 and TRPC6 were present at normal levels. |
| 1242 | 23948707 | OAG also increased steady-state surface expression of the NOX2 regulatory subunit p47(phox). |
| 1243 | 23948707 | In whole cell recordings, TRPC6 activation by OAG was reduced in podocytes pretreated with the NOX2 inhibitor apocynin, by the pan-NOX inhibitor diphenylene iodonium, and by tempol, a ROS quencher. |
| 1244 | 23948707 | These data suggest that active NOX2 assembles with TRPC6 at podocin-organized sterol-rich raft domains and becomes catalytically active in response to DAG. |
| 1245 | 23948707 | NOX2 interacts with podocyte TRPC6 channels and contributes to their activation by diacylglycerol: essential role of podocin in formation of this complex. |
| 1246 | 23948707 | TRPC6 channels are typically activated by diacylglycerol (DAG) during PLC-dependent transduction cascades. |
| 1247 | 23948707 | We previously showed that podocin is required for DAG analogs to produce robust activation of TRPC6 channels in podocytes. |
| 1248 | 23948707 | Here we show that endogenous TRPC6 channels in immortalized podocytes reciprocally coimmunoprecipitate with the catalytic subunit of the NADPH oxidase NOX2 (gp91(phox)). |
| 1249 | 23948707 | The NOX2-TRPC6 interaction was not detected in cells stably expressing a short hairpin RNA targeting podocin, although NOX2 and TRPC6 were present at normal levels. |
| 1250 | 23948707 | OAG also increased steady-state surface expression of the NOX2 regulatory subunit p47(phox). |
| 1251 | 23948707 | In whole cell recordings, TRPC6 activation by OAG was reduced in podocytes pretreated with the NOX2 inhibitor apocynin, by the pan-NOX inhibitor diphenylene iodonium, and by tempol, a ROS quencher. |
| 1252 | 23948707 | These data suggest that active NOX2 assembles with TRPC6 at podocin-organized sterol-rich raft domains and becomes catalytically active in response to DAG. |
| 1253 | 23977013 | Isolated LP glomeruli show a reduced level of miR-200a, miR-141, miR-429 and ZEB2 mRNA and upregulated collagen 1α1/2 mRNA expression. |
| 1254 | 23977013 | By western blot analyzes of whole kidney tissue, we found significant reduction of both podocin and nephrin and enhanced expression of mesenchymal protein markers such as desmin, collagen type I and fibronectin. |
| 1255 | 24069045 | Rapamycin ameliorates proteinuria and restores nephrin and podocin expression in experimental membranous nephropathy. |
| 1256 | 24137241 | Furthermore, the glomerular hypertrophy and foot process effacement were improved, and there was a recovery of the slit diaphragm associated with nephrin and podocin expression. |
| 1257 | 24137241 | Furthermore, triptolide significantly reduced the expression of transforming growth factor-β1 and osteopontin, and the infiltration of ED-1-positive cells into the kidney. |
| 1258 | 24173355 | Macrophage depletion in diabetic CD11b-DTR mice significantly attenuated albuminuria, kidney macrophage recruitment, and glomerular histological changes and preserved kidney nephrin and podocin expression compared with diabetic CD11b-DTR mice treated with mutant DT. |
| 1259 | 24195695 | The present study sought to determine whether doses of ARB (AngII receptor blocker) that maximally reduce proteinuria could slow the progression of glomerulosclerosis in the uninephrectomized db/db mouse, a model of Type 2 diabetes. |
| 1260 | 24195695 | Untreated uninephrectomized db/db mice had normal blood pressure, but developed progressive albuminuria and mesangial matrix expansion between 18 and 22 weeks of age, which was associated with increased renal expression of TGFβ1 (transforming growth factor β1), PAI-1 (plasminogen-activator inhibitor-1), type IV collagen and FN (fibronectin). |
| 1261 | 24195695 | The expression of podocin and nephrin were continually decreased in mice with diabetes between 18 and 22 weeks of age. |
| 1262 | 24195695 | Renal expression of TNFα (tumour necrosis factor α), MCP-1 (monocyte chemoattractant protein-1), Nox2 (NADPH oxidase 2), p22phox and p47phox and urine TBARS (thiobarbituric acid-reacting substance) levels, the markers of renal inflammation and oxidative stress, were increased during disease progression in mice with diabetes. |
| 1263 | 24260371 | Synaptopodin and podocin expression was reduced as well as nephrin protein, particularly in the SRL group. |
| 1264 | 24260371 | NFκB activation and IL-6 levels were lower in EVL and SRL, and even lower in SRL. |
| 1265 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1266 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1267 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1268 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1269 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1270 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1271 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1272 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1273 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1274 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1275 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1276 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1277 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1278 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1279 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1280 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1281 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1282 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1283 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1284 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1285 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1286 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1287 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1288 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1289 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1290 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1291 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1292 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1293 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1294 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1295 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1296 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1297 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1298 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1299 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1300 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1301 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1302 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1303 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1304 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1305 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1306 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1307 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1308 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1309 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1310 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1311 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1312 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1313 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1314 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1315 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1316 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1317 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1318 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1319 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1320 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1321 | 24337247 | Nephrin and Podocin functions are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1322 | 24337247 | Zebrafish Nephrin and Podocin are important in the formation of the podocyte SD and mutations in NEPHRIN and PODOCIN genes cause human nephrotic syndrome. |
| 1323 | 24337247 | To understand the function of Podocin and Nephrin in zebrafish, splice‑blocking morpholino antisense oligonucleotides were used. |
| 1324 | 24337247 | Knockdown of Podocin or Nephrin by this method induced pronephric glomerular hypoplasia with pericardial edema. |
| 1325 | 24337247 | Human Nephrin and Podocin mRNA rescued this glomerular phenotype, however, the efficacy of the rescues was greatly reduced when mRNA‑encoding human disease‑causing NEPHRIN‑R1109X and PODOCIN‑R138Q were used. |
| 1326 | 24337247 | Furthermore, an association between zebrafish Nephrin and Podocin proteins was observed. |
| 1327 | 24337247 | Notably, Podocin‑R150Q, corresponding to human PODOCIN‑R138Q, markedly interacted with Nephrin compared with wild‑type Podocin, suggesting that this strong binding capacity of mutated Podocin impairs the transport of Nephrin and Podocin out of the endoplasmic reticulum. |
| 1328 | 24337247 | The results suggest that the functions of Nephrin and Podocin are highly conserved between the zebrafish pronephros and mammalian metanephros. |
| 1329 | 24443353 | Untreated uninephrectomized db/db mice developed significant mesangial matrix expansion and albuminuria at week 22 of age, associated with segmental podocyte foot-process effacement, reduction of renal nephrin, podocin and zonula occludin-1 production and induction of renal desmin and B7-1 generation. |
| 1330 | 24443353 | Importantly, recombinant PAI-1 downregulated nephrin and zonula occludin-1 but increased desmin and B7-1 mRNA expression and protein production by podocytes in vitro, similar to the effects of transforming growth factor-β1. |
| 1331 | 24443353 | These observations provide evidence that PAI-1, in a manner similar to transforming growth factor-β1, directly induces podocyte injury, particularly in the setting of diabetes, where elevated PAI-1 may contribute to the progression of albuminuria. |
| 1332 | 24454919 | In addition, both puerarin and losartan increased expression of podocyte slit diaphragm proteins such as nephrin and podocin. |
| 1333 | 24461191 | Among the identified genes mutated in podocytes include NPHS2, NPHS1, WT1, TRPC6, MDR1, PLCE1, LMX1B, and LAMB2. |
| 1334 | 24468088 | IgA-HMC medium prepared with pIgA from IgAN, lead to obvious fibrogenic activation, evidenced by the loss of Podocin and CD2AP in podocytes, loss of E-cadherin and Megalin in HK2 cells and increase of FN and Col I in both cells. miR-21 targeted PTEN in these cells. |
| 1335 | 24468088 | Inhibition of miR-21 preserved the expression of PTEN, prevented the activation of Akt and inhibited the fibrogenic activation in podocytes and HK2 cells exposed to the IgA-HMC medium prepared with pIgA from IgAN. |
| 1336 | 24468088 | In conclusion, our study suggests that inhibition of miR-21 prevents fibrogenic activation in podocytes and tubular cells by preventing PTEN/Akt pathway activation in IgAN. |
| 1337 | 24511133 | The prohibitin homology domain of the slit diaphragm protein podocin contained one such site, threonine 234 (T234), located within a phosphorylation motif that is mutated in human genetic forms of proteinuria. |
| 1338 | 24533170 | High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway. |
| 1339 | 24533170 | (Pro)renin receptor (PRR) expression is upregulated in diabetes. |
| 1340 | 24533170 | We hypothesized that PRR contributes to podocyte injury via activation of Wnt-β-catenin-snail signaling pathway. |
| 1341 | 24533170 | Compared to normal glucose, high glucose significantly decreased mRNA and protein expressions of podocin and nephrin, and increased mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail, respectively. |
| 1342 | 24533170 | Cells treated with high glucose and PRR siRNA demonstrated significantly attenuated mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail; enhanced expressions of podocin mRNA and protein, improved expression and reorganization of F-actin, and reduced transwell albumin flux. |
| 1343 | 24533170 | High glucose induces podocyte injury via enhanced (pro)renin receptor-Wnt-β-catenin-snail signaling pathway. |
| 1344 | 24533170 | (Pro)renin receptor (PRR) expression is upregulated in diabetes. |
| 1345 | 24533170 | We hypothesized that PRR contributes to podocyte injury via activation of Wnt-β-catenin-snail signaling pathway. |
| 1346 | 24533170 | Compared to normal glucose, high glucose significantly decreased mRNA and protein expressions of podocin and nephrin, and increased mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail, respectively. |
| 1347 | 24533170 | Cells treated with high glucose and PRR siRNA demonstrated significantly attenuated mRNA and protein expressions of PRR, Wnt3a, β-catenin, and snail; enhanced expressions of podocin mRNA and protein, improved expression and reorganization of F-actin, and reduced transwell albumin flux. |
| 1348 | 24559085 | Podocin and beta dystroglycan expression to study podocyte-podocyte and basement membrane matrix connections in adult protienuric states. |
| 1349 | 24647714 | There was a paradoxical increase in CoRL in the intraglomerular compartment at 52 and 64 wk of age, where a subset coexpressed the podocyte proteins nephrin, podocin, and synaptopodin. |
| 1350 | 24699703 | Studies have shown that some mature proteins of podocytes, such as podocin, nephrin, and synaptopodin, were also expressed in neurons. |
| 1351 | 24699703 | We further inhibited the expression of Neuron-specific enolase, nestin, synaptopodin and Ubiquitin carboxy terminal hydrolase-1 by Small interfering RNA in cultured mouse podocytes and observed the significant morphological changes in treated podocytes. |
| 1352 | 24699703 | When podocytes were treated with Adriamycin, the protein expression of Neuron-specific enolase, nestin, synaptopodin and Ubiquitin carboxy terminal hydrolase-1 decreased over time. |
| 1353 | 24722437 | Stimulation of primary mouse podocytes with endothelin-1 elicited rapid calcium transients mediated by endothelin type A receptors (ETARs) and endothelin type B receptors (ETBRs). |
| 1354 | 24722437 | We then generated mice with a podocyte-specific double deletion of ETAR and ETBR (NPHS2-Cre×Ednra(lox/lox)×Ednrb(lox/lox) [Pod-ETRKO]). |
| 1355 | 24722437 | In vitro, treatment with endothelin-1 increased total β-catenin and phospho-NF-κB expression in wild-type glomeruli, but this effect was attenuated in Pod-ETRKO glomeruli. |
| 1356 | 24722437 | This evidence suggests that endothelin-1 drives development of glomerulosclerosis and podocyte loss through direct activation of endothelin receptors and NF-κB and β-catenin pathways in podocytes. |
| 1357 | 24722440 | Osr1 deficiency in mice results in metanephric kidney agenesis, whereas knockdown or mutation studies in zebrafish revealed that pronephric nephrons require osr1 for proximal tubule and podocyte development. osr1-deficient pronephric podocyte progenitors express the Wilms' tumor suppressor wt1a but do not undergo glomerular morphogenesis or express the foot process junctional markers nephrin and podocin. |
| 1358 | 24722440 | Furthermore, unlike the osr1-deficient proximal tubule phenotype, which can be rescued by manipulation of endoderm development, podocyte differentiation was not affected by altered endoderm development, as assessed by nephrin and podocin expression in double osr1/sox32-deficient embryos. |
| 1359 | 24722440 | Indeed, osr1-deficient embryos did not exhibit podocyte progenitor expression of the transcription factor lhx1a, and forced expression of activated forms of the lhx1a gene product rescued nephrin expression in osr1-deficient podocytes. |
| 1360 | 24722440 | Our results place osr1 in a framework of transcriptional regulators that control the expression of podocin and nephrin and thereby mediate podocyte differentiation. |
| 1361 | 24722440 | Osr1 deficiency in mice results in metanephric kidney agenesis, whereas knockdown or mutation studies in zebrafish revealed that pronephric nephrons require osr1 for proximal tubule and podocyte development. osr1-deficient pronephric podocyte progenitors express the Wilms' tumor suppressor wt1a but do not undergo glomerular morphogenesis or express the foot process junctional markers nephrin and podocin. |
| 1362 | 24722440 | Furthermore, unlike the osr1-deficient proximal tubule phenotype, which can be rescued by manipulation of endoderm development, podocyte differentiation was not affected by altered endoderm development, as assessed by nephrin and podocin expression in double osr1/sox32-deficient embryos. |
| 1363 | 24722440 | Indeed, osr1-deficient embryos did not exhibit podocyte progenitor expression of the transcription factor lhx1a, and forced expression of activated forms of the lhx1a gene product rescued nephrin expression in osr1-deficient podocytes. |
| 1364 | 24722440 | Our results place osr1 in a framework of transcriptional regulators that control the expression of podocin and nephrin and thereby mediate podocyte differentiation. |
| 1365 | 24722440 | Osr1 deficiency in mice results in metanephric kidney agenesis, whereas knockdown or mutation studies in zebrafish revealed that pronephric nephrons require osr1 for proximal tubule and podocyte development. osr1-deficient pronephric podocyte progenitors express the Wilms' tumor suppressor wt1a but do not undergo glomerular morphogenesis or express the foot process junctional markers nephrin and podocin. |
| 1366 | 24722440 | Furthermore, unlike the osr1-deficient proximal tubule phenotype, which can be rescued by manipulation of endoderm development, podocyte differentiation was not affected by altered endoderm development, as assessed by nephrin and podocin expression in double osr1/sox32-deficient embryos. |
| 1367 | 24722440 | Indeed, osr1-deficient embryos did not exhibit podocyte progenitor expression of the transcription factor lhx1a, and forced expression of activated forms of the lhx1a gene product rescued nephrin expression in osr1-deficient podocytes. |
| 1368 | 24722440 | Our results place osr1 in a framework of transcriptional regulators that control the expression of podocin and nephrin and thereby mediate podocyte differentiation. |
| 1369 | 24808537 | Using MPC5 immortalized mouse podocytes, ADR dose dependently induced downregulation of nephrin and podocin, cell apoptosis, and mitochondrial dysfunction based on the increase in mitochondrial ROS production, decrease in mitochondrial DNA copy number, and reduction of mitochondrial membrane potential and ATP content. |
| 1370 | 24808537 | Strikingly, PGC-1α overexpression markedly attenuated mitochondrial dysfunction, the reduction of nephrin and podocin, and the apoptotic response in podocytes after ADR treatment. |
| 1371 | 24808537 | Using MPC5 immortalized mouse podocytes, ADR dose dependently induced downregulation of nephrin and podocin, cell apoptosis, and mitochondrial dysfunction based on the increase in mitochondrial ROS production, decrease in mitochondrial DNA copy number, and reduction of mitochondrial membrane potential and ATP content. |
| 1372 | 24808537 | Strikingly, PGC-1α overexpression markedly attenuated mitochondrial dysfunction, the reduction of nephrin and podocin, and the apoptotic response in podocytes after ADR treatment. |
| 1373 | 24827776 | In diabetic mice, deletion of the CB2 receptor albuminuria, the downregulation of podocin and nephrin, mesangial expansion, overexpression of extracellular matrix components, monocyte infiltration, and reduced renal function were all exacerbated. |
| 1374 | 24827776 | Absence of CB2 on resident glomerular cells had a major role in worsening diabetic nephropathy, both functional and structural abnormalities, likely by enhanced MCP-1 and CB1 signaling. |
| 1375 | 24846581 | The protein/mRNA expression of podocin, nephrin, transforming growth factor β1(TGF-β1), and the RARs (RAR-α,β,γ) was measured by RT-PCR and Western blotting. |
| 1376 | 24846581 | Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-β1 (all p < 0.05). |
| 1377 | 24846581 | The RAR-α/γ protein expression level was positively correlated with nephrin and podocin (-α, r = 0.637, 0.663; -γ, r = 0.882, 0.878; all p < 0.05), and negatively correlated with TGF-β1 (-α, r = -0.650; -γ, r = -0.739; all p < 0.05). |
| 1378 | 24846581 | The RAR-β protein expression level was not correlated with nephrin, podocin and TGF-β1 (r = -0.312, 0.079, -0.279; all p > 0.05). |
| 1379 | 24846581 | The protein/mRNA expression of podocin, nephrin, transforming growth factor β1(TGF-β1), and the RARs (RAR-α,β,γ) was measured by RT-PCR and Western blotting. |
| 1380 | 24846581 | Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-β1 (all p < 0.05). |
| 1381 | 24846581 | The RAR-α/γ protein expression level was positively correlated with nephrin and podocin (-α, r = 0.637, 0.663; -γ, r = 0.882, 0.878; all p < 0.05), and negatively correlated with TGF-β1 (-α, r = -0.650; -γ, r = -0.739; all p < 0.05). |
| 1382 | 24846581 | The RAR-β protein expression level was not correlated with nephrin, podocin and TGF-β1 (r = -0.312, 0.079, -0.279; all p > 0.05). |
| 1383 | 24846581 | The protein/mRNA expression of podocin, nephrin, transforming growth factor β1(TGF-β1), and the RARs (RAR-α,β,γ) was measured by RT-PCR and Western blotting. |
| 1384 | 24846581 | Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-β1 (all p < 0.05). |
| 1385 | 24846581 | The RAR-α/γ protein expression level was positively correlated with nephrin and podocin (-α, r = 0.637, 0.663; -γ, r = 0.882, 0.878; all p < 0.05), and negatively correlated with TGF-β1 (-α, r = -0.650; -γ, r = -0.739; all p < 0.05). |
| 1386 | 24846581 | The RAR-β protein expression level was not correlated with nephrin, podocin and TGF-β1 (r = -0.312, 0.079, -0.279; all p > 0.05). |
| 1387 | 24846581 | The protein/mRNA expression of podocin, nephrin, transforming growth factor β1(TGF-β1), and the RARs (RAR-α,β,γ) was measured by RT-PCR and Western blotting. |
| 1388 | 24846581 | Compared with the injured podocytes, ATRA exposure significantly increased the protein/mRNA expression of nephrin and podocin and it markedly reduced TGF-β1 (all p < 0.05). |
| 1389 | 24846581 | The RAR-α/γ protein expression level was positively correlated with nephrin and podocin (-α, r = 0.637, 0.663; -γ, r = 0.882, 0.878; all p < 0.05), and negatively correlated with TGF-β1 (-α, r = -0.650; -γ, r = -0.739; all p < 0.05). |
| 1390 | 24846581 | The RAR-β protein expression level was not correlated with nephrin, podocin and TGF-β1 (r = -0.312, 0.079, -0.279; all p > 0.05). |
| 1391 | 24850187 | Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. |
| 1392 | 24850187 | Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin. |
| 1393 | 24850187 | Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. |
| 1394 | 24850187 | Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin. |
| 1395 | 24854274 | Lmx1b and FoxC combinatorially regulate podocin expression in podocytes. |
| 1396 | 24854274 | We found that the NPHS2 promoter also contains a cis-acting Lmx1b-FoxC motif that binds LMX1B and FoxC2. |
| 1397 | 24854274 | Among these candidates, motif-driven podocyte enhancer activity of CCNC and MEIS2 was functionally analyzed in vivo. |
| 1398 | 24854274 | Lmx1b and FoxC combinatorially regulate podocin expression in podocytes. |
| 1399 | 24854274 | We found that the NPHS2 promoter also contains a cis-acting Lmx1b-FoxC motif that binds LMX1B and FoxC2. |
| 1400 | 24854274 | Among these candidates, motif-driven podocyte enhancer activity of CCNC and MEIS2 was functionally analyzed in vivo. |
| 1401 | 24858365 | These effects appeared to be due to the maintained expression of nephrin and podocin on podocytes as well as the reduced expression of profibrotic factors like transforming growth factor-β (TGF-β). |
| 1402 | 24904088 | Tcf21 was deleted from podocytes and podocyte progenitors using podocin-cre (podTcf21) and wnt4-cre (wnt4creTcf21) driver strains, respectively. |
| 1403 | 24926327 | The expression levels of nephrin and podocin were evaluated using immunofluorescence staining. |
| 1404 | 24926327 | The high cortical expression of nephrin and podocin protein decreased. |
| 1405 | 24926327 | The glomeruli, tubules and podocytes exhibited pathomorphological improvements and the nephrin and podocin protein expression levels were higher in the nephridial tissue. |
| 1406 | 24926327 | The expression levels of nephrin and podocin were evaluated using immunofluorescence staining. |
| 1407 | 24926327 | The high cortical expression of nephrin and podocin protein decreased. |
| 1408 | 24926327 | The glomeruli, tubules and podocytes exhibited pathomorphological improvements and the nephrin and podocin protein expression levels were higher in the nephridial tissue. |
| 1409 | 24926327 | The expression levels of nephrin and podocin were evaluated using immunofluorescence staining. |
| 1410 | 24926327 | The high cortical expression of nephrin and podocin protein decreased. |
| 1411 | 24926327 | The glomeruli, tubules and podocytes exhibited pathomorphological improvements and the nephrin and podocin protein expression levels were higher in the nephridial tissue. |
| 1412 | 24954247 | Immunofluorescence staining of the slit diaphragm protein podocin and the tight junction protein ZO-1 revealed a partial mislocalization of these proteins. |
| 1413 | 24963322 | YQQRG inhibited VEGF-A, nephrin, podocin, and CD2AP mRNA expression and elevated nephrin, podocin, and CD2AP protein levels starting on day 3. |
| 1414 | 24963322 | In conclusion, YQQRG attenuates podocyte injury in the rat PAN model through downregulation of VEGF-A and restoration of nephrin, podocin, and CD2AP protein expression. |
| 1415 | 24963322 | YQQRG inhibited VEGF-A, nephrin, podocin, and CD2AP mRNA expression and elevated nephrin, podocin, and CD2AP protein levels starting on day 3. |
| 1416 | 24963322 | In conclusion, YQQRG attenuates podocyte injury in the rat PAN model through downregulation of VEGF-A and restoration of nephrin, podocin, and CD2AP protein expression. |
| 1417 | 25012166 | Multiple genes of the renin-angiotensin system are novel targets of Wnt/β-catenin signaling. |
| 1418 | 25012166 | By bioinformatics analyses, we discovered that the promoter regions of all RAS genes contained putative T-cell factor (TCF)/lymphoid enhancer factor (LEF)-binding sites, and β-catenin induced the binding of LEF-1 to these sites in kidney tubular cells. |
| 1419 | 25012166 | Moreover, ICG-001 therapy restored expression of nephrin, podocin, and Wilms' tumor 1, attenuated interstitial myofibroblast activation, repressed matrix expression, and inhibited renal inflammation and fibrosis. |
| 1420 | 25092178 | The effects of Ang-(1-7) on the expression of podocyte-specific proteins [nephrin, Wilms tumor‑1 (WT-1) and podocin] and the phosphorylation of mitogen-activated protein kinases (MAPKs) were investigated by western blot analysis. |
| 1421 | 25092178 | The results revealed that in the cultured podocytes incubated with preeclamptic serum, there was a decrease in the expression of podocyte-specific proteins (nephrin and WT-1 but not podocin), a rearrangement of F-actin and apoptosis compared with the control group. |
| 1422 | 25092178 | However, treatment with Ang-(1-7) attenuated podocyte injury in the preeclamptic group, which may be mediated through the downregulation of MAPK (p38, ERK1/2 and JNK) phosphorylation. |
| 1423 | 25092178 | The effects of Ang-(1-7) on the expression of podocyte-specific proteins [nephrin, Wilms tumor‑1 (WT-1) and podocin] and the phosphorylation of mitogen-activated protein kinases (MAPKs) were investigated by western blot analysis. |
| 1424 | 25092178 | The results revealed that in the cultured podocytes incubated with preeclamptic serum, there was a decrease in the expression of podocyte-specific proteins (nephrin and WT-1 but not podocin), a rearrangement of F-actin and apoptosis compared with the control group. |
| 1425 | 25092178 | However, treatment with Ang-(1-7) attenuated podocyte injury in the preeclamptic group, which may be mediated through the downregulation of MAPK (p38, ERK1/2 and JNK) phosphorylation. |
| 1426 | 25138219 | In cultured podocytes, size exclusion chromatography and confocal microscopy showed that inhibition of TXNIP by siRNA or verapamil prevented Hcys-induced TXNIP protein recruitment to form NLRP3 inflammasomes and abolished Hcys-induced increases in caspase-1 activity and IL-1β production. |
| 1427 | 25138219 | TXNIP inhibition protected podocytes from injury as shown by normal expression levels of podocyte markers, podocin and desmin. |
| 1428 | 25138219 | Furthermore, TXNIP inhibition significantly reduced caspase-1 activity and IL-1β production in glomeruli of mice with hHcys. |
| 1429 | 25182410 | Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. |
| 1430 | 25182410 | Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. |
| 1431 | 25182410 | Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression. |
| 1432 | 25182410 | Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. |
| 1433 | 25182410 | Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. |
| 1434 | 25182410 | Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression. |
| 1435 | 25182410 | Upregulation of Galectin-1 is associated with loss of podocin, which is important for the physiological function of podocytes and decreases in the renal tissues of diabetic nephropathy. |
| 1436 | 25182410 | Increased Galectin-1 is a causal event for the high glucose-induced loss of podocin, since silencing Galectin-1 in podocytes increased podocin expression in the presence of 25 mM glucose. |
| 1437 | 25182410 | Thus expression of Galectin-1 in diabetic nephropathy may serve as a marker and contribute to disease progression by interfering with podocin expression. |
| 1438 | 25188527 | Calcitriol, a bioactive 1,25-dihydroxyvitamin D3, ameliorated proteinuria and renal damage as well as reversed the decline of both nephrin and podocin, crucial structural proteins in podocytes. |
| 1439 | 25188527 | Interestingly, calcitriol promoted M2 macrophage activation with enhanced expression of CD163, arginase-1, and mannose receptor at week 18 but not at week 8 or 14. |
| 1440 | 25188527 | The ratio of CD163 to CD68, considered as the proportion of M2 macrophages, was about 2.9-fold higher at week 18 after calcitriol treatment. |
| 1441 | 25188527 | Furthermore, the protein expression of inducible nitric oxide synthase, a crucial marker of M1 macrophages, was negatively correlated with the expression of either nephrin or podocin, whereas CD163, indicating M2 macrophages, was positively correlated. |
| 1442 | 25188527 | Calcitriol, a bioactive 1,25-dihydroxyvitamin D3, ameliorated proteinuria and renal damage as well as reversed the decline of both nephrin and podocin, crucial structural proteins in podocytes. |
| 1443 | 25188527 | Interestingly, calcitriol promoted M2 macrophage activation with enhanced expression of CD163, arginase-1, and mannose receptor at week 18 but not at week 8 or 14. |
| 1444 | 25188527 | The ratio of CD163 to CD68, considered as the proportion of M2 macrophages, was about 2.9-fold higher at week 18 after calcitriol treatment. |
| 1445 | 25188527 | Furthermore, the protein expression of inducible nitric oxide synthase, a crucial marker of M1 macrophages, was negatively correlated with the expression of either nephrin or podocin, whereas CD163, indicating M2 macrophages, was positively correlated. |
| 1446 | 25199697 | Interestingly, cinnamon and its PCB2-fraction prevented the AGE mediated loss of expression of glomerular podocyte proteins; nephrin and podocin. |
| 1447 | 25244654 | In mice exposed to indoxyl sulfate for 2 h, isolated glomeruli manifested increased Cyp1a1 expression, indicating AhR activation. |
| 1448 | 25244654 | After 8 w of indoxyl sulfate, podocytes showed foot process effacement, cytoplasmic vacuoles, and a focal granular and wrinkled pattern of podocin and synaptopodin expression. |
| 1449 | 25244654 | Furthermore, vimentin and AhR expression in the glomerulus was increased in the indoxyl sulfate-exposed glomeruli compared to controls. |
| 1450 | 25244654 | Glomerular expression of characteristic podocyte mRNAs was decreased, including Actn4, Cd2ap, Myh9, Nphs1, Nphs2, Podxl, Synpo, and Wt1. |
| 1451 | 25244654 | In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. |
| 1452 | 25244654 | In mice exposed to indoxyl sulfate for 2 h, isolated glomeruli manifested increased Cyp1a1 expression, indicating AhR activation. |
| 1453 | 25244654 | After 8 w of indoxyl sulfate, podocytes showed foot process effacement, cytoplasmic vacuoles, and a focal granular and wrinkled pattern of podocin and synaptopodin expression. |
| 1454 | 25244654 | Furthermore, vimentin and AhR expression in the glomerulus was increased in the indoxyl sulfate-exposed glomeruli compared to controls. |
| 1455 | 25244654 | Glomerular expression of characteristic podocyte mRNAs was decreased, including Actn4, Cd2ap, Myh9, Nphs1, Nphs2, Podxl, Synpo, and Wt1. |
| 1456 | 25244654 | In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. |
| 1457 | 25292315 | Meanwhile, in DN rats, the expression of podocyte specific markers including nephrin and podocin was significantly decreased, accompanied by increased desmin, a marker of podocyte injury. |
| 1458 | 25292315 | In contrast, TRPC6 was negatively correlated with both VDR and nephrin expression in podocytes. |
| 1459 | 25420462 | We discovered several phosphorylation sites with potentially high biological relevance, e.g. tyrosine phosphorylation of the cytoskeletal regulator synaptopodin and the slit diaphragm protein neph-1 (Kirrel). |
| 1460 | 25420462 | Moreover, cross-species comparisons revealed conserved phosphorylation of the slit diaphragm protein nephrin on an acidic cluster at the intracellular terminus and conserved podocin phosphorylation on the very carboxyl terminus of the protein. |
| 1461 | 25420462 | We studied a highly conserved podocin phosphorylation site in greater detail and show that phosphorylation regulates affinity of the interaction with nephrin and CD2AP. |
| 1462 | 25420462 | We discovered several phosphorylation sites with potentially high biological relevance, e.g. tyrosine phosphorylation of the cytoskeletal regulator synaptopodin and the slit diaphragm protein neph-1 (Kirrel). |
| 1463 | 25420462 | Moreover, cross-species comparisons revealed conserved phosphorylation of the slit diaphragm protein nephrin on an acidic cluster at the intracellular terminus and conserved podocin phosphorylation on the very carboxyl terminus of the protein. |
| 1464 | 25420462 | We studied a highly conserved podocin phosphorylation site in greater detail and show that phosphorylation regulates affinity of the interaction with nephrin and CD2AP. |
| 1465 | 25422468 | In cultured human podocytes, CB1R and desmin gene expression were increased and podocin and nephrin content were decreased by either the CB1R agonist arachydonoyl-2'-chloroethylamide, angiotensin II, or high glucose, and the effects of all three were antagonized by CB1R blockade or siRNA-mediated knockdown of CNR1 (the cannabinoid type 1 receptor gene). |
| 1466 | 25460740 | Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported. |
| 1467 | 25460740 | These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria. |
| 1468 | 25460740 | Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP. |
| 1469 | 25460740 | Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs. |
| 1470 | 25460740 | Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported. |
| 1471 | 25460740 | These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria. |
| 1472 | 25460740 | Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP. |
| 1473 | 25460740 | Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs. |
| 1474 | 25460740 | Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported. |
| 1475 | 25460740 | These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria. |
| 1476 | 25460740 | Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP. |
| 1477 | 25460740 | Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs. |
| 1478 | 25468389 | In BXSB-Yaa mice, the glomerular levels of Tlr8 mRNA negatively correlated with the glomerular levels of podocyte functional markers (Nphs1, Nphs2, and Synpo) and positively correlated with urinary albumin levels. |
| 1479 | 25468389 | Furthermore, the glomerular and serum levels of miR-21, a putative microRNA ligand of TLR8, were higher in BXSB-Yaa mice than in BXSB mice. |
| 1480 | 25501161 | Recent studies have demonstrated that mutations in 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1, are associated with the pathogenesis of steroid-resistant nephrotic syndrome (SRNS). |
| 1481 | 25501161 | We analyzed mutations in the 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1. |
| 1482 | 25501161 | Of the 20 SRNS children showing complete remission who responded to prolonged steroid therapy or immunosuppressive agents, 4 heterozygous NPHS1 mutations, 928G>A, IVS8+30C>T, IVS21+14G>A, and IVS25-23C>T, were identified in 4 patients and a heterozygous CD2AP mutation, IVS7-135G>A, was identified in 1 patient. |
| 1483 | 25501161 | Recent studies have demonstrated that mutations in 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1, are associated with the pathogenesis of steroid-resistant nephrotic syndrome (SRNS). |
| 1484 | 25501161 | We analyzed mutations in the 4 podocyte genes, NPHS1, NPHS2, CD2AP, and WT1. |
| 1485 | 25501161 | Of the 20 SRNS children showing complete remission who responded to prolonged steroid therapy or immunosuppressive agents, 4 heterozygous NPHS1 mutations, 928G>A, IVS8+30C>T, IVS21+14G>A, and IVS25-23C>T, were identified in 4 patients and a heterozygous CD2AP mutation, IVS7-135G>A, was identified in 1 patient. |
| 1486 | 25556170 | Integration of Cistromic and Transcriptomic Analyses Identifies Nphs2, Mafb, and Magi2 as Wilms' Tumor 1 Target Genes in Podocyte Differentiation and Maintenance. |
| 1487 | 25556170 | The Wilms' tumor suppressor gene 1 (WT1) encodes a zinc finger transcription factor. |
| 1488 | 25556170 | To address the evolutionary conservation of WT1 targets, we performed functional assays using zebrafish as a model and identified Nphs2, Mafb, and Magi2 as novel WT1 target genes required for podocyte development. |
| 1489 | 25556170 | Our data also show that both Mafb and Magi2 are required for normal development of the embryonic zebrafish kidney. |
| 1490 | 25676004 | We focus on the staining gap (podocin gap) defined as the staining difference between podocin and synaptopodin, which are normally located in the foot process. |
| 1491 | 25861251 | Following the Huaier treatment, the notable downregulation of PGC-1α and its downstream molecule mitochondrial transcription factor A (TFAM) were almost entirely blocked. |
| 1492 | 25861251 | Correspondingly, Huaier markedly ameliorated ADR-induced podocyte injury and mitochondrial dysfunction in both rat kidneys and incubated cells as it inhibited the decrease of nephrin and podocin expression, mtDNA copy number, MMP, and ATP content. |
| 1493 | 25892536 | Immunohistochemistry also revealed decreased and altered expression of nephrin and podocin in the glomeruli compared with normal canine glomeruli. |
| 1494 | 25892536 | These results suggested that the glomerular disease of the present case might be consistent with canine hereditary nephropathy resembling human Alport syndrome caused by genetic defect of type IV collagen, and indicated possible contribution of podocyte injury to severe proteinuria in this case. |
| 1495 | 25986755 | Observation by electronic microscope revealed structural damage of podocytes; the reduced expression level of podocyte marker genes, nephrin and podocin, was also detected by q-PCR. |
| 1496 | 25986755 | Moreover, AT2R gene and protein expressions in fetal kidneys were inhibited by PCE, associated with the repression of the gene expression of glial-cell-line-derived neurotrophic factor (GDNF)/tyrosine kinase receptor (c-Ret) signaling pathway. |
| 1497 | 26038526 | In older age podocyte detachment rate (urine podocin mRNA-to-creatinine ratio) was higher than at younger ages and podocytes were stressed (increased urine podocin-to-nephrin mRNA ratio). |
| 1498 | 26116357 | Intravital Imaging Reveals Angiotensin II-Induced Transcytosis of Albumin by Podocytes. |
| 1499 | 26116357 | We recently showed that angiotensin II (Ang II) acutely increases albumin filtration in the healthy kidney. |
| 1500 | 26116357 | Acute infusion of 30, 60, or 80 ng/kg per minute Ang II enhanced the endocytosis of albumin by activation of the type 1 Ang II receptor and resulted in an average (±SEM) of 3.7±2.2, 72.3±18.6 (P<0.001), and 239.4±34.6 µm(3) (P<0.001) albumin-containing vesicles per glomerulus, respectively, compared with none at baseline or 10 ng/kg per minute Ang II. |
| 1501 | 26116357 | Immunostaining of Ang II-infused kidneys confirmed the presence of albumin-containing vesicles, which colocalized with megalin, in podocin-positive cells. |
| 1502 | 26116357 | Furthermore, podocyte endocytosis of albumin was markedly reduced in the presence of gentamicin, a competitive inhibitor of megalin-dependent endocytosis. |
| 1503 | 26116357 | Ang II infusion increased the concentration of albumin in the subpodocyte space, a potential source for endocytic protein uptake, and gentamicin further increased this concentration. |
| 1504 | 26116357 | Ang II enhances the endocytosis and transcytosis of plasma albumin by podocytes, which may eventually impair podocyte function. |
| 1505 | 26155842 | In addition, we observed a decreased expression of podocin and overexpression of monocyte chemoattractant protein-1 and fibrotic-related markers, including transforming growth factor-β1, Col1a1, and α-smooth muscle actin. |
| 1506 | 26156092 | Recent advances show that human focal segmental glomerulosclerosis (FSGS) is a primary podocytopathy caused by podocyte-specific gene mutations including NPHS1, NPHS2, WT-1, LAMB2, CD2AP, TRPC6, ACTN4 and INF2. |
| 1507 | 26160898 | The proteins sensing mechanical forces in podocytes are unconfirmed, but the classic transient receptor potential channel 6 (TRPC6) interacting with the MEC-2 homolog podocin may form a mechanosensitive ion channel complex in podocytes. |
| 1508 | 26160898 | However, TRPC6-deficient podocytes responded in a manner similar to that of control podocytes, and mechanically induced currents were unaffected by genetic inactivation of TRPC1/3/6 or administration of the broad-range TRPC blocker SKF-96365. |
| 1509 | 26160898 | Moreover, mechanical P2X4 channel activation depended on cholesterol and podocin and was inhibited by stabilization of the actin cytoskeleton. |
| 1510 | 26160898 | The proteins sensing mechanical forces in podocytes are unconfirmed, but the classic transient receptor potential channel 6 (TRPC6) interacting with the MEC-2 homolog podocin may form a mechanosensitive ion channel complex in podocytes. |
| 1511 | 26160898 | However, TRPC6-deficient podocytes responded in a manner similar to that of control podocytes, and mechanically induced currents were unaffected by genetic inactivation of TRPC1/3/6 or administration of the broad-range TRPC blocker SKF-96365. |
| 1512 | 26160898 | Moreover, mechanical P2X4 channel activation depended on cholesterol and podocin and was inhibited by stabilization of the actin cytoskeleton. |
| 1513 | 26175845 | A feedback increase in renin production often accompanies angiotensin II blockade. |
| 1514 | 26175845 | We therefore examined whether aliskiren, a direct renin inhibitor, confers better renoprotection than angiotensin II blockade and whether the addition of aliskiren to an ACEI or ARB would enhance the efficacy in slowing the progression of glomerulosclerosis in diabetes. |
| 1515 | 26175845 | Untreated db/db mice developed progressive mesangial matrix expansion and albuminuria between weeks 18 and 22, associated with reduction of WT-1 immunopositive podocytes and nephrin and podocin production and induction of desmin and B7-1 generation and renal expression of TGFß1, PAI-1, fibronectin and type IV collagen. |
| 1516 | 26175845 | Combined therapy caused the loss of 10% ~ 16.6% of db/db mice, yielded no further reduction in renal fibrosis and podocyte injury but further reduced albuminuria and renal production of TNFα, Nox2 and p47phox and urine MCP-1 and malondialdehyde levels, the markers of renal inflammation and oxidative stress. |
| 1517 | 26195484 | Glomerular nephrin, Neph1, podocin, and endothelin-converting enzyme gene expression were downregulated in a dose-dependent manner. |
| 1518 | 26234796 | Role of the heme oxygenase-adiponectin-atrial natriuretic peptide axis in renal function. |
| 1519 | 26234796 | The mechanisms underlying the HO-mediated reno-protection include: (i) the restoration of renal morphology by enhancing proteins of regeneration, (ii) the potentiation of the HO-adiponectin-atrial natriuretic peptide axis, with corresponding suppression of oxidative/inflammatory insults and extracellular matrix/profibrotic factors, and (iii) the potentiation of podocyte cytoskeletal proteins such as nephrin, podocin, podocalyxin and CD2-associated-protein, which are fundamental for forming the glomerular filtration barrier that selectively allows small molecules to pass through but not large protein molecules. |
| 1520 | 26234796 | Thus, this review highlights the HO-adiponectin-atrial natriuretic peptide axis in renoprotection. |
| 1521 | 26248309 | In comparison, DBA/2J mice developed albuminuria on similar diets, signs of fibrosis, oxidative stress, early signs of podocyte loss (evaluated by the markers podocin and WT-1) and podocyte insulin resistance (unable to phosphorylate their glomerular Akt when insulin was given). |
| 1522 | 26293507 | Notch1 and Notch2 in Podocytes Play Differential Roles During Diabetic Nephropathy Development. |
| 1523 | 26293507 | Here, we report that conditional deletion of Notch1 in podocytes using NPHS2(cre)Notch1(flox/flox) animals resulted in marked amelioration of DKD. |
| 1524 | 26293507 | Deletion of Notch1 in podocytes also resulted in an increase in Notch2 expression, indicating an interaction between the receptors. |
| 1525 | 26293507 | At the same time, transgenic overexpression of Notch2 in podocytes did not induce phenotypic changes, while constitutive expression of Notch1 caused rapid development of albuminuria and glomerulosclerosis. |
| 1526 | 26309060 | Immunohistochemical microscopic findings of the expressions of FSP-1 and WT-1 (two glomerular damage indicators) and KIM-1 and snail (two renal tubular-damaged indicators) showed an identical pattern, whereas the expressions of ZO-1, p-cadherin, podocin, dystroglycan, fibronectin, and synaptopodin (six indices of glomerular integrity) demonstrated an opposite pattern compared to that of PIS among five groups (all P < 0.001). |
| 1527 | 26309060 | Protein expressions of inflammatory (TNF-α/NF-κB/MMP-9) and oxidative stress (NOX-1, NOX-2, oxidized protein) biomarkers exhibited an identical pattern to that of PIS among five groups (all P < 0.001). |
| 1528 | 26522148 | The expression levels of podocyte-specific proteins, nephrin, podocin, and synaptopodin were decreased in the MSHRSP/Kpo glomeruli, though another podocyte-specific protein, CD2AP, in the MSHRSP/Kpo glomeruli exhibited a similar extent of staining as in normotensive WKY/Kpo rats. |
| 1529 | 26539236 | Cellular experiments in vitro showed that curcumin significantly antagonized leptin-induced downregulation of the mRNA and protein expression of podocyte-associated molecules including nephrin, podocin, podoplanin, and podocalyxin. |
| 1530 | 26539236 | Furthermore, the experiments in vitro and in vivo both displayed that curcumin could downregulate the mRNA and protein expressions of Wnt1, Wnt2b, Wnt6, and β-catenin and upregulate the phosphorylation level of β-catenin protein in podocytes and renal tissue. |
| 1531 | 26550253 | After 8-week treatment, the rats of each group were killed for the renal functional and pathological detection, as well as the expression detection of nephrin and podocin of kidney tissues. |
| 1532 | 26550253 | Meanwhile, the expressions of nephrin/podocin were reduced (P<0.05); among which group B exhibited the most serious changes, while the situations of group E were improved after the combined treatment, the expressions of nephrin/podocin were increased. |
| 1533 | 26550253 | Low-dose rapamycin and valsartan could enhance the expressions of nephrin and podocin, reduce kidney damages, thus achieving the protective effects towards the kidneys, and the effects of the combined therapy were superior to those of monotherapy. |
| 1534 | 26550253 | After 8-week treatment, the rats of each group were killed for the renal functional and pathological detection, as well as the expression detection of nephrin and podocin of kidney tissues. |
| 1535 | 26550253 | Meanwhile, the expressions of nephrin/podocin were reduced (P<0.05); among which group B exhibited the most serious changes, while the situations of group E were improved after the combined treatment, the expressions of nephrin/podocin were increased. |
| 1536 | 26550253 | Low-dose rapamycin and valsartan could enhance the expressions of nephrin and podocin, reduce kidney damages, thus achieving the protective effects towards the kidneys, and the effects of the combined therapy were superior to those of monotherapy. |
| 1537 | 26550253 | After 8-week treatment, the rats of each group were killed for the renal functional and pathological detection, as well as the expression detection of nephrin and podocin of kidney tissues. |
| 1538 | 26550253 | Meanwhile, the expressions of nephrin/podocin were reduced (P<0.05); among which group B exhibited the most serious changes, while the situations of group E were improved after the combined treatment, the expressions of nephrin/podocin were increased. |
| 1539 | 26550253 | Low-dose rapamycin and valsartan could enhance the expressions of nephrin and podocin, reduce kidney damages, thus achieving the protective effects towards the kidneys, and the effects of the combined therapy were superior to those of monotherapy. |
| 1540 | 26566632 | FK506 reduces albuminuria through improving podocyte nephrin and podocin expression in diabetic rats. |
| 1541 | 26628676 | By immunoblotting, we found that several urinary serine proteases were significantly increased in CHF rats compared with sham rats (fold increases: furin 6.7, prostasin 23.6, plasminogen 2.06, and plasmin 3.57 versus sham). |
| 1542 | 26628676 | Consistent with these results, podocyte damage markers desmin and podocin expressions were also increased in rats with CHF (increased ≈2-folds). |
| 1543 | 26632605 | In the human study, focal segmental glomerulosclerosis (FSGS) patients presented with higher levels of urinary AGT, corrected by UP, than minimal-change disease (MCD) patients. |
| 1544 | 26632605 | Furthermore, AGT was evident in podocin-negative glomerular segmental lesions. |
| 1545 | 26632605 | The urinary AGT/UP ratio and AGT protein and mRNA expression in sieved glomeruli from FSGS rats were significantly higher than in MCD rats. |
| 1546 | 26632605 | Finally, we observed the renal tissue and urinary metabolism of exogenous injected human recombinant AGT (which is not cleaved by rodent renin) in FSGS and control rats. |
| 1547 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 1548 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 1549 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 1550 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 1551 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 1552 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 1553 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 1554 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 1555 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 1556 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 1557 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 1558 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 1559 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 1560 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 1561 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 1562 | 26728561 | Alport syndrome (AS) is a hereditary glomerulopathy caused by a mutation in type IV collagen genes, which disrupts glomerular basement membrane, leading to progressive glomerulosclerosis and end-stage renal failure. |
| 1563 | 26728561 | This was associated with less renal cortical fibrosis and interstitial inflammation compared to nontransplanted mice as shown by reduction in murine CD4, CD68, and CD45.2 cells. |
| 1564 | 26728561 | Transplanted CSC homed to glomeruli, where they expressed CR1, VEGFA, SYNAPTOPODIN, CD2AP, and PODOCIN at the RNA level and produced PODOCIN, CD2AP, and COLIVα3 proteins in nontransplanted -/- mice, indicating that CSC have adopted a podocyte phenotype. |
| 1565 | 26739892 | Interestingly, inhibition of mPGES-1 with a small interfering RNA approach significantly attenuated ADR-induced downregualtion of podocin and nephrin. |
| 1566 | 26739892 | In agreement with the improvement of cell phenotypic alteration and apoptosis, the enhanced inflammatory markers of IL-1β and TNF-α were also significantly suppressed by mPGES-1 silencing. |
| 1567 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1568 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1569 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1570 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1571 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1572 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1573 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1574 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1575 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1576 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1577 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1578 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1579 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1580 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1581 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1582 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1583 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1584 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1585 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1586 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1587 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1588 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1589 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1590 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1591 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1592 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1593 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1594 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1595 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1596 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1597 | 26770424 | Effect of simvastatin on the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF) in podocytes of diabetic rat. |
| 1598 | 26770424 | Renal pathological changes were observed, and immunohistochemistry was performed to determine the expression of nephrin, podocin, and vascular endothelial growth factor (VEGF). |
| 1599 | 26770424 | Real-time PCR was performed to detect the mRNA expression levels of nephrin, podocin, and VEGF. |
| 1600 | 26770424 | The protein and mRNA expression levels of nephrin and podocin were lower in the DM group than in the NC group (P < 0.01); whereas, the expression of VEGF protein and mRNA was higher in the DM group than in the NC group (P < 0.01). |
| 1601 | 26770424 | Simvastatin (SVT) could reduce serum creatinine levels and the UAER, maintain the expression of nephrin and podocin, reduce the expression of VEGF, and improve the pathological changes of podocytes, which were much more pronounced at 8 weeks (P < 0.01). |
| 1602 | 26770424 | Simvastatin could maintain the distribution of nephrin and podocin in podocytes, inhibit VEGF expression, and thus improve podocyte injuries and protect kidney functions in diabetic rats. |
| 1603 | 26792065 | We also found that activation of Rac1 in podocytes significantly downregulated the expression of nephrin and podocin, suggesting an adverse effect of Rac1 on slit diaphragm protein expression. |
| 1604 | 26792178 | The ubiquitin ligase Ubr4 controls stability of podocin/MEC-2 supercomplexes. |
| 1605 | 26792178 | The PHB-domain protein podocin maintains the renal filtration barrier and its mutation is an important cause of hereditary nephrotic syndrome. |
| 1606 | 26792178 | Here, we show that the ubiquitin ligase Ubr4 is a key component of the podocin interactome purified both from cultured podocytes and native glomeruli. |
| 1607 | 26792178 | The ubiquitin ligase Ubr4 controls stability of podocin/MEC-2 supercomplexes. |
| 1608 | 26792178 | The PHB-domain protein podocin maintains the renal filtration barrier and its mutation is an important cause of hereditary nephrotic syndrome. |
| 1609 | 26792178 | Here, we show that the ubiquitin ligase Ubr4 is a key component of the podocin interactome purified both from cultured podocytes and native glomeruli. |
| 1610 | 26792178 | The ubiquitin ligase Ubr4 controls stability of podocin/MEC-2 supercomplexes. |
| 1611 | 26792178 | The PHB-domain protein podocin maintains the renal filtration barrier and its mutation is an important cause of hereditary nephrotic syndrome. |
| 1612 | 26792178 | Here, we show that the ubiquitin ligase Ubr4 is a key component of the podocin interactome purified both from cultured podocytes and native glomeruli. |
| 1613 | 26823550 | Furthermore, both podocin and nephrin, two essential components of the slit diaphragm, translocated to Rab7- and lysosome-associated membrane glycoprotein 1-positive amphisomes/autolysosomes that accumulated in podocyte cell bodies in podocyte-specific CD-knockout mice. |
| 1614 | 26851346 | Expression of nephrin, podocin, desmin, and transient receptor potential channel C6 in the podocyte was significantly altered in 1,25-vitamin D3-deficient animals. |
| 1615 | 26851346 | The effect of 1,25-vitamin D3 deficiency and 1,25-vitamin D3 and 1,25-vitamin D2 repletion on proteinuria could not be explained by hypocalcemia, changes in parathyroid hormone, or fibroblast growth factor 23. |
| 1616 | 26854253 | Phospholipase A2 receptor (PLA2R) expressed in human podocytes has been highlighted as a causative autoantigen of human idiopathic membranous nephropathy. |
| 1617 | 26854253 | The cultured cells expressed PLA2R mRNA and protein in addition to other podocyte markers (synaptopodin, podocin and nephrin). |
| 1618 | 26889414 | Many of the proteins within the slit diaphragm, including nephrin, podocin, transient receptor potential-6 channel, and α-actinin-4, have been identified via genetic studies of inherited nephrotic syndromes. |
| 1619 | 26902315 | Further, EA also prevented the AGE-mediated loss of expression of podocyte slit diaphragm proteins: nephrin and podocin. |
| 1620 | 27052160 | Seventy-seven and 116 pelleted urine samples from 38 and 18 women at various stages of normal and PE pregnancies, respectively underwent quantitative analysis of podocyte-specific or associated protein mRNA expression, including podocin, nephrin, and synaptopodin using RT-PCR. |
| 1621 | 27052160 | The podocin:nephrin mRNA ratio (PNR) and synaptopodin:nephrin mRNA ratio (SNR) increased significantly with increasing P/Cr, while the podocin:synaptopodin mRNA ratio (PSR) did not change significantly according to P/Cr, resulting in significantly higher PNR and SNR, but not PSR levels, in urine from PE women with than without SPIP. |
| 1622 | 27052160 | Seventy-seven and 116 pelleted urine samples from 38 and 18 women at various stages of normal and PE pregnancies, respectively underwent quantitative analysis of podocyte-specific or associated protein mRNA expression, including podocin, nephrin, and synaptopodin using RT-PCR. |
| 1623 | 27052160 | The podocin:nephrin mRNA ratio (PNR) and synaptopodin:nephrin mRNA ratio (SNR) increased significantly with increasing P/Cr, while the podocin:synaptopodin mRNA ratio (PSR) did not change significantly according to P/Cr, resulting in significantly higher PNR and SNR, but not PSR levels, in urine from PE women with than without SPIP. |
| 1624 | 27076646 | On FSGS day 7, immunostaining for the podocyte markers p57, synaptopodin, and podocin were markedly decreased by 44%, and this was accompanied by a decrease in ZsGreen fluorescence. |
| 1625 | 27076646 | Staining for p57, synaptopodin, podocin, and DAPI increased at FSGS day 28 and was augmented by the ACE inhibitor enalapril, which is consistent with a partial replenishment of podocytes. |
| 1626 | 27076646 | Moreover, more than half of the migrated podocytes coexpressed the parietal epithelial cell (PEC) proteins claudin-1, SSeCKS, and PAX8. |
| 1627 | 27076646 | On FSGS day 7, immunostaining for the podocyte markers p57, synaptopodin, and podocin were markedly decreased by 44%, and this was accompanied by a decrease in ZsGreen fluorescence. |
| 1628 | 27076646 | Staining for p57, synaptopodin, podocin, and DAPI increased at FSGS day 28 and was augmented by the ACE inhibitor enalapril, which is consistent with a partial replenishment of podocytes. |
| 1629 | 27076646 | Moreover, more than half of the migrated podocytes coexpressed the parietal epithelial cell (PEC) proteins claudin-1, SSeCKS, and PAX8. |
| 1630 | 27102209 | Thus, this study was undertaken to investigate whether amylin aggregation stimulates the local angiotensin II type 1 receptor (AT1R) in podocytes, and to examine its role in podocyte apoptosis. |
| 1631 | 27102209 | Expression of genes including nephrin, podocin, AT1R and desmin was measured through quantitative real time PCR, western blot and immunohistochemistry. |
| 1632 | 27102209 | Apoptosis was determined by flow cytometry, while the cellular distribution of podocin and nephrin was investigated by immunofluorescence. |
| 1633 | 27102209 | The peptide also suppressed podocin and nephrin expression, but enhanced that of AT1R and desmin. |
| 1634 | 27102209 | Thus, this study was undertaken to investigate whether amylin aggregation stimulates the local angiotensin II type 1 receptor (AT1R) in podocytes, and to examine its role in podocyte apoptosis. |
| 1635 | 27102209 | Expression of genes including nephrin, podocin, AT1R and desmin was measured through quantitative real time PCR, western blot and immunohistochemistry. |
| 1636 | 27102209 | Apoptosis was determined by flow cytometry, while the cellular distribution of podocin and nephrin was investigated by immunofluorescence. |
| 1637 | 27102209 | The peptide also suppressed podocin and nephrin expression, but enhanced that of AT1R and desmin. |
| 1638 | 27102209 | Thus, this study was undertaken to investigate whether amylin aggregation stimulates the local angiotensin II type 1 receptor (AT1R) in podocytes, and to examine its role in podocyte apoptosis. |
| 1639 | 27102209 | Expression of genes including nephrin, podocin, AT1R and desmin was measured through quantitative real time PCR, western blot and immunohistochemistry. |
| 1640 | 27102209 | Apoptosis was determined by flow cytometry, while the cellular distribution of podocin and nephrin was investigated by immunofluorescence. |
| 1641 | 27102209 | The peptide also suppressed podocin and nephrin expression, but enhanced that of AT1R and desmin. |
| 1642 | 27105734 | Loss of the stomatin/PHB/flotillin/HflK/C (SPFH) domain containing protein PHB2 causes mitochondrial dysfunction and defective mitochondria-mediated signaling, which is implicated in a variety of human diseases, including progressive renal disease. |
| 1643 | 27105734 | PHB2 coprecipitated with podocin, another SPFH domain-containing protein, essential for the assembly of the slit diaphragm protein-lipid supercomplex. |
| 1644 | 27105734 | Consistent with an evolutionarily conserved extra-mitochondrial function, the ortholog of PHB2 in Caenorhabditis elegans was also not restricted to mitochondria but colocalized with the mechanosensory complex that requires the podocin ortholog MEC2 for assembly. |
| 1645 | 27105734 | Loss of the stomatin/PHB/flotillin/HflK/C (SPFH) domain containing protein PHB2 causes mitochondrial dysfunction and defective mitochondria-mediated signaling, which is implicated in a variety of human diseases, including progressive renal disease. |
| 1646 | 27105734 | PHB2 coprecipitated with podocin, another SPFH domain-containing protein, essential for the assembly of the slit diaphragm protein-lipid supercomplex. |
| 1647 | 27105734 | Consistent with an evolutionarily conserved extra-mitochondrial function, the ortholog of PHB2 in Caenorhabditis elegans was also not restricted to mitochondria but colocalized with the mechanosensory complex that requires the podocin ortholog MEC2 for assembly. |
| 1648 | 27114314 | The present study was designed to determine the mechanism underlying the treatment of nephrotic syndrome using astragaloside by observing the effects of astragaloside on the expression of nephrin and podocin proteins and genes in kidneys of rats with adriamycin nephropathy. |
| 1649 | 27114314 | The mRNA expression of nephrin and podocin was measured in the kidney tissues using the real-time qPCR, and the protein expression levels of nephrin and podocin were detected using Western blot analysis. |
| 1650 | 27114314 | The nephrin and podocin mRNA and protein expression levels in the intervention groups were higher (P < 0.05) than that in the model group. |
| 1651 | 27114314 | Due to the increased expression of podocyte-related nephrin and podocin proteins, astragaloside maintained slit diaphragm integrity and decreased the level of proteinuria in rats with adriamycin nephropathy. |
| 1652 | 27114314 | The present study was designed to determine the mechanism underlying the treatment of nephrotic syndrome using astragaloside by observing the effects of astragaloside on the expression of nephrin and podocin proteins and genes in kidneys of rats with adriamycin nephropathy. |
| 1653 | 27114314 | The mRNA expression of nephrin and podocin was measured in the kidney tissues using the real-time qPCR, and the protein expression levels of nephrin and podocin were detected using Western blot analysis. |
| 1654 | 27114314 | The nephrin and podocin mRNA and protein expression levels in the intervention groups were higher (P < 0.05) than that in the model group. |
| 1655 | 27114314 | Due to the increased expression of podocyte-related nephrin and podocin proteins, astragaloside maintained slit diaphragm integrity and decreased the level of proteinuria in rats with adriamycin nephropathy. |
| 1656 | 27114314 | The present study was designed to determine the mechanism underlying the treatment of nephrotic syndrome using astragaloside by observing the effects of astragaloside on the expression of nephrin and podocin proteins and genes in kidneys of rats with adriamycin nephropathy. |
| 1657 | 27114314 | The mRNA expression of nephrin and podocin was measured in the kidney tissues using the real-time qPCR, and the protein expression levels of nephrin and podocin were detected using Western blot analysis. |
| 1658 | 27114314 | The nephrin and podocin mRNA and protein expression levels in the intervention groups were higher (P < 0.05) than that in the model group. |
| 1659 | 27114314 | Due to the increased expression of podocyte-related nephrin and podocin proteins, astragaloside maintained slit diaphragm integrity and decreased the level of proteinuria in rats with adriamycin nephropathy. |
| 1660 | 27114314 | The present study was designed to determine the mechanism underlying the treatment of nephrotic syndrome using astragaloside by observing the effects of astragaloside on the expression of nephrin and podocin proteins and genes in kidneys of rats with adriamycin nephropathy. |
| 1661 | 27114314 | The mRNA expression of nephrin and podocin was measured in the kidney tissues using the real-time qPCR, and the protein expression levels of nephrin and podocin were detected using Western blot analysis. |
| 1662 | 27114314 | The nephrin and podocin mRNA and protein expression levels in the intervention groups were higher (P < 0.05) than that in the model group. |
| 1663 | 27114314 | Due to the increased expression of podocyte-related nephrin and podocin proteins, astragaloside maintained slit diaphragm integrity and decreased the level of proteinuria in rats with adriamycin nephropathy. |
| 1664 | 27122542 | Moreover, its homolog Pard3b, and not Pard3a, is the dominant Par3 gene expressed in podocytes and found at the basis of the slit diaphragm, where it partially colocalizes with podocin. |
| 1665 | 27151920 | In diabetic nephropathy, the gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, accompanied by a tighter filtration slit and the appearance of TJ-like structures between the foot processes. |
| 1666 | 27151920 | However, there is no definitive evidence to show slit diaphragm (SD) to TJ transition in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-inducible transgene expression specifically in the glomerular podocyte. |
| 1667 | 27151920 | We found that induction of claudin-1 gene expression in mature podocytes caused profound proteinuria, and with deep-etching freeze-fracture electron microscopy, we resolved the ultrastructural change in the claudin-1-induced SD-TJ transition. |
| 1668 | 27151920 | Notably, immunolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex in podocytes, with significantly reduced expression and altered localization of nephrin and podocin proteins. |
| 1669 | 27151920 | Mechanistically, claudin-1 interacted with both nephrin and podocin through cis- and trans-associations in cultured cells. |
| 1670 | 27151920 | Furthermore, the rat puromycin aminonucleoside nephrosis model, previously suspected of undergoing SD-TJ transition, exhibited upregulated expression levels of claudin-1 mRNA and protein in podocytes. |
| 1671 | 27151920 | In diabetic nephropathy, the gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, accompanied by a tighter filtration slit and the appearance of TJ-like structures between the foot processes. |
| 1672 | 27151920 | However, there is no definitive evidence to show slit diaphragm (SD) to TJ transition in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-inducible transgene expression specifically in the glomerular podocyte. |
| 1673 | 27151920 | We found that induction of claudin-1 gene expression in mature podocytes caused profound proteinuria, and with deep-etching freeze-fracture electron microscopy, we resolved the ultrastructural change in the claudin-1-induced SD-TJ transition. |
| 1674 | 27151920 | Notably, immunolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex in podocytes, with significantly reduced expression and altered localization of nephrin and podocin proteins. |
| 1675 | 27151920 | Mechanistically, claudin-1 interacted with both nephrin and podocin through cis- and trans-associations in cultured cells. |
| 1676 | 27151920 | Furthermore, the rat puromycin aminonucleoside nephrosis model, previously suspected of undergoing SD-TJ transition, exhibited upregulated expression levels of claudin-1 mRNA and protein in podocytes. |
| 1677 | 27153922 | Furthermore, DOCA treatment led to decreased expression of the slit diaphragm-associated proteins podocin, nephrin, and synaptopodin and to enhanced transient receptor potential canonical 6 (TRPC6) channel expression and ATP-induced calcium influx in podocytes of Podo-GC-A KO mice. |
| 1678 | 27174202 | GLCCI1 is a novel component associated with the PI3K signaling pathway in podocyte foot processes. |
| 1679 | 27174202 | The main objective of this study was to investigate the regulation of podocyte foot process proteins and to investigate the role of GLCCI1 in the phosphoinositide 3-kinase (PI3K) pathway using high glucose-induced podocytes and streptozotocin-induced diabetic rats. |
| 1680 | 27174202 | In podocytes and rat kidneys, GLCCI1 was found to be highly specific for the glomerulus and podocyte foot processes similar to other podocyte-specific proteins (nephrin, podocin, synatopodin and podocalyxin) based on reverse transcription-PCR, western blotting, immunofluorescence and immunoelectron microscopy analyses. |
| 1681 | 27174202 | In addition, the decrease in the GLCCI1 expression level under hyperglycemic conditions was restored by treatment with a PI3K inhibitor (wortmannin). |
| 1682 | 27174202 | Immunofluorescence analysis confirmed that GLCCI1 colocalized with nephrin and synaptopodin both in vivo and in vitro. |
| 1683 | 27174202 | Hence, GLCCI1 is a component of podocyte foot processes, and its expression appears to be regulated via the PI3K pathway. |
| 1684 | 27186971 | Furthermore, the protein expression, including podocin, nephrin, and synaptopodin was down-regulated by the TM treatment in the MPC5 cells. |
| 1685 | 27193387 | Podocin, an integral membrane protein belonging to stomatin family, is expressed exclusively in podocytes and is localized to slit-diaphragm (SD). |
| 1686 | 27221629 | The expression levels of light chain 3‑II (LC3 II), beclin‑1, P62, CCAAT‑enhancer‑binding protein homologous protein (CHOP) and podocin were determined by western blot analysis. |
| 1687 | 27221629 | Furthermore, the autophagy enhancer rapamycin reversed the downregulation of LC3 II and podocin, and the upregulation of CHOP induced by LPS, while the autophagy inhibitor 3‑MA aggravated the effects of LPS. |
| 1688 | 27221629 | The expression levels of light chain 3‑II (LC3 II), beclin‑1, P62, CCAAT‑enhancer‑binding protein homologous protein (CHOP) and podocin were determined by western blot analysis. |
| 1689 | 27221629 | Furthermore, the autophagy enhancer rapamycin reversed the downregulation of LC3 II and podocin, and the upregulation of CHOP induced by LPS, while the autophagy inhibitor 3‑MA aggravated the effects of LPS. |
| 1690 | 27255369 | Further investigations via immunofluorescence staining, real-time reverse transcription polymerase chain reaction and Western blot analysis showed that the decreased slit diaphragm protein nephrin and podocin mRNA expression and protein levels in DN mice were restored by hyperoside treatment. |
| 1691 | 27273997 | In MCD mouse model and human kidney tissues, the expressions of podocyte slit membrane protein-nephrin and podocin, skeleton protein-synaptopodin are decreased, and the expression of synaptopodin is correlated with the response to hormone therapy. |
| 1692 | 27273997 | In addition, newest studies focused on another two potocyte associated proteins, CD80 and Angiopoietin-like-4. |
| 1693 | 27273997 | Angiopoietin-like-4 can be expressed in normal potocytes, but over-expression of angiopoietin-like-4 may injure the GBM charge barrier and induce the foot process fusion, leading to MCD. |
| 1694 | 27273997 | However, further studies on the factors inducing CD80 and Angiopoietin-like-4 expression, and the interaction between glomerular basement membrane and the two proteins are needed. |
| 1695 | 27273997 | Based on the mechanism of MCD, NF-kappa B inhibitors and sialylation therapy would be a novel non-immune therapy for MCD. |
| 1696 | 27312386 | Additionally, MPA can inhibit apoptosis in podocytes and seems to be beneficial in preserving the expression of nephrin and podocin, and by attenuation of urokinase receptor expression leads to decreased foot-process effacement. |
| 1697 | 27350175 | INF2 interacts directly with certain other mammalian diaphanous formin proteins (mDia) that function as RhoA effector molecules. |
| 1698 | 27350175 | FSGS-causing INF2 mutations impair these interactions and disrupt the ability of INF2 to regulate Rho/Dia-mediated actin dynamics in vitro. |
| 1699 | 27350175 | This is associated with persistent podocyte cytoplasmic aggregation, nephrin phosphorylation, and nephrin and podocin mislocalization, as well as impaired recovery of mDia membrane localization. |
| 1700 | 27357417 | The expression levels of epithelial markers, including nephrin, podocin and synaptopodin, were decreased by HG and increased by BIO, whereas the reverse were true for mesenchymal markers, including α‑smooth muscle actin (α‑SMA) and fibronectin. |
| 1701 | 27357417 | In conclusion, the present study revealed that the mechanism by which BIO inhibited HG‑mediated EMT in podocytes and the renal cortex was primarily due to the VDR. |
| 1702 | 27403197 | The proteins expressions of podocin, nephrin, collagen IV, and fibronectin (FN) were examined by immunohistochemical staining, and key proteins involved in TGF-β/Smad signaling were evaluated by RT-PCR and western blotting. |
| 1703 | 27403197 | JWDG decoction also inhibited the expression of the collagen IV, FN, and fibrogenic TGF-β. |
| 1704 | 27406771 | These NPHS2-Angptl4 transgenic rats over-express two different forms of the glycoprotein Angptl4 from the podocyte. |
| 1705 | 27442391 | Hildebrandt's group has shown that 85% of the SRNS cases with onset by 3 months of age and 66% with onset by 1 year of age can be explained by recessive mutations in one of four genes only (NPHS1, NPHS2, LAMB2, or WT1). |
| 1706 | 27442391 | This is very important for patients who carry mutations in a gene of coenzyme Q10 biosynthesis (COQ2, COQ6, ADCK4, or PDSS2). |
| 1707 | 27462276 | Restoration of renal function in HF rats by DPPIV inhibition was associated with increased active glucagon-like peptide-1 (GLP-1) serum concentration, reduced DPPIV activity and increased activity of protein kinase A in the renal cortex. |
| 1708 | 27462276 | Furthermore, the anti-proteinuric effect of vildagliptin treatment in rats with established HF was associated with upregulation of the apical proximal tubule endocytic receptor megalin and of the podocyte main slit diaphragm proteins nephrin and podocin. |
| 1709 | 27571993 | Notoginsenoside R1 ameliorates podocyte injury in rats with diabetic nephropathy by activating the PI3K/Akt signaling pathway. |
| 1710 | 27571993 | Pathological staining was performed to evaluate the renal protective effect of NR1, and the expression of the key slit diaphragm proteins, namely neprhin, podocin and desmin, were evaluated. |
| 1711 | 27571993 | In addition, the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), tumor growth factor-β1 (TGF-β1), interleukin (IL)-1 and IL-6] as well as an anti-inflammatory cytokine (IL-10) were assessed, and the apoptosis of podocytes was quantified. |
| 1712 | 27571993 | Finally, the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and the involvement of nuclear factor-κB (NF-κB) inactivation was further analyzed. |
| 1713 | 27571993 | In this study, NR1 improved renal function by ameliorating histological alterations, increasing the expression of nephrin and podocin, decreasing the expression of desmin, and inhibiting both the inflammatory response as well as the apoptosis of podocytes. |
| 1714 | 27571993 | Furthermore, NR1 treatment increased the phosphorylation of both PI3K (p85) and Akt, indicating that activation of the PI3K/Akt signaling pathway was involved. |
| 1715 | 27571993 | This is the first study to the best of our knowledge, to clearly demonstrate that NR1 treatment ameliorates podocyte injury by inhibiting both inflammation and apoptosis through the PI3K/Akt signaling pathway. |
| 1716 | 27571993 | Notoginsenoside R1 ameliorates podocyte injury in rats with diabetic nephropathy by activating the PI3K/Akt signaling pathway. |
| 1717 | 27571993 | Pathological staining was performed to evaluate the renal protective effect of NR1, and the expression of the key slit diaphragm proteins, namely neprhin, podocin and desmin, were evaluated. |
| 1718 | 27571993 | In addition, the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), tumor growth factor-β1 (TGF-β1), interleukin (IL)-1 and IL-6] as well as an anti-inflammatory cytokine (IL-10) were assessed, and the apoptosis of podocytes was quantified. |
| 1719 | 27571993 | Finally, the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway and the involvement of nuclear factor-κB (NF-κB) inactivation was further analyzed. |
| 1720 | 27571993 | In this study, NR1 improved renal function by ameliorating histological alterations, increasing the expression of nephrin and podocin, decreasing the expression of desmin, and inhibiting both the inflammatory response as well as the apoptosis of podocytes. |
| 1721 | 27571993 | Furthermore, NR1 treatment increased the phosphorylation of both PI3K (p85) and Akt, indicating that activation of the PI3K/Akt signaling pathway was involved. |
| 1722 | 27571993 | This is the first study to the best of our knowledge, to clearly demonstrate that NR1 treatment ameliorates podocyte injury by inhibiting both inflammation and apoptosis through the PI3K/Akt signaling pathway. |
| 1723 | 27580845 | Our results showed that CsA and FK506 treatment decreased proteinuria via a mechanism associated to a reduction in the foot-process fusion and desmin, and a recovery of synaptopodin and podocin. |
| 1724 | 27580845 | In PAN-treated mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cytoskeleton, increased the expression of synaptopodin and podocin, improved podocyte viability, and reduced the migrating activities of podocytes. |
| 1725 | 27580845 | Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, which was associated with the induction of Bcl-xL and inhibition of Bax, cleaved caspase 3, and cleaved PARP expression. |
| 1726 | 27580845 | Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signaling, thereby protecting podocytes from PAN-induced injury. |
| 1727 | 27630573 | TRPC6 activation by 20-HETE was eliminated in cells pretreated with TEMPOL, a membrane-permeable superoxide dismutase mimic. |
| 1728 | 27630573 | Responses to 20-HETE were eliminated by siRNA knockdown of podocin, a protein that organizes NADPH oxidase complexes with TRPC6 subunits in this cell type. |
| 1729 | 27633396 | Secondly, knockdown of HDAC9 in mouse podocytes significantly suppressed HG-induced reactive oxygen species (ROS) generation, cell apoptosis and inflammation through JAK2/STAT3 pathway and reduced the podocytes injury by decreasing the expression levels of Nephrin and Podocin. |
| 1730 | 27704688 | FAK contributes to proteinuria in hypercholesterolaemic rats and modulates podocyte F-actin re-organization via activating p38 in response to ox-LDL. |
| 1731 | 27704688 | FAK is also an adaptor protein initiating cascades of intracellular signals including c-Src, Rho GTPase and mitogen-activated protein kinase (MAPK). |
| 1732 | 27704688 | Our cell culture data revealed oxidized low-density lipoprotein (ox-LDL) triggered hyper-phosphorylation of FAK and p38, ectopic expression of cellular markers (manifested as decreased WT1, podocin and NEPH1, and increased vimentin and mmp9), and re-arrangement of F-actin filaments with enhanced cell motility; these mutations were significantly rectified by FAK shRNA. |
| 1733 | 27704688 | Notably, pre-treatment of p38 inhibitor did not alter FAK activation, albeit its deletion of p38 hyper-activity and attenuation of cellular abnormalities, demonstrating that p38 acted as a downstream effector of FAK signalling and ox-LDL damaged podocytes in a FAK/p38-dependent manner. |
| 1734 | 27704688 | This was further identified by animal data that p38 activation was also abrogated by TAE226 treatment in hypercholesterolaemic rats, suggesting that FAK/p38 axis might also be involved in in vivo events. |
| 1735 | 27748847 | The expression levels of the epithelial cell markers, nephrin and podocin, and the myofibroblast cell markers, α‑smooth muscle actin (SMA) and fibronectin, in podocytes by western blot analysis and immunofluorescence staining, respectively. |
| 1736 | 27748847 | It was observed that HG promotes EMT in podocytes, due to the increased levels of podocin and nephrin expression and the reduced α‑SMA and fibronectin expression levels. |
| 1737 | 27748847 | The expression levels of the epithelial cell markers, nephrin and podocin, and the myofibroblast cell markers, α‑smooth muscle actin (SMA) and fibronectin, in podocytes by western blot analysis and immunofluorescence staining, respectively. |
| 1738 | 27748847 | It was observed that HG promotes EMT in podocytes, due to the increased levels of podocin and nephrin expression and the reduced α‑SMA and fibronectin expression levels. |
| 1739 | 27823966 | The linear regression analysis found the optical density of IFIT1 was inversely associated with F-actin, Nephrin, and Podocin, but not Synatopodin. |
| 1740 | 27885584 | WT1 and NPHS2 gene mutation analysis and clinical management of steroid-resistant nephrotic syndrome. |
| 1741 | 27885584 | Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1). |
| 1742 | 27885584 | NPHS1, NPHS2, and WT1 genes are identified/directly linked to SRNS. |
| 1743 | 27885584 | The present study is a surveillance on the mutation analysis of WT1 (exons 8 and 9) and NPHS2 (exons 1-8) gene in SRNS followed by clinical management. |
| 1744 | 27885584 | WT1 and NPHS2 gene mutation analysis and clinical management of steroid-resistant nephrotic syndrome. |
| 1745 | 27885584 | Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1). |
| 1746 | 27885584 | NPHS1, NPHS2, and WT1 genes are identified/directly linked to SRNS. |
| 1747 | 27885584 | The present study is a surveillance on the mutation analysis of WT1 (exons 8 and 9) and NPHS2 (exons 1-8) gene in SRNS followed by clinical management. |
| 1748 | 27885584 | WT1 and NPHS2 gene mutation analysis and clinical management of steroid-resistant nephrotic syndrome. |
| 1749 | 27885584 | Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1). |
| 1750 | 27885584 | NPHS1, NPHS2, and WT1 genes are identified/directly linked to SRNS. |
| 1751 | 27885584 | The present study is a surveillance on the mutation analysis of WT1 (exons 8 and 9) and NPHS2 (exons 1-8) gene in SRNS followed by clinical management. |
| 1752 | 27885584 | WT1 and NPHS2 gene mutation analysis and clinical management of steroid-resistant nephrotic syndrome. |
| 1753 | 27885584 | Non-responsiveness of these children would be a risk with the possibility of mutational changes in podocyte genes (NPHS1, NPHS2, WT1, PLCE1). |
| 1754 | 27885584 | NPHS1, NPHS2, and WT1 genes are identified/directly linked to SRNS. |
| 1755 | 27885584 | The present study is a surveillance on the mutation analysis of WT1 (exons 8 and 9) and NPHS2 (exons 1-8) gene in SRNS followed by clinical management. |
| 1756 | 27887947 | The results indicated that berberine significantly mitigated high glucose-decreased cell viability, and nephrin and podocin expression as well as apoptosis in mouse podocytes. |
| 1757 | 27887947 | Furthermore, berberine significantly increased the high glucose-elevated Unc-51-like autophagy-activating kinase 1 (ULK1) S317/S555 phosphorylation, Beclin-1 expression, the ratios of LC3II to LC3I expression and the numbers of autophagosomes, but reduced ULK1 S757 phosphorylation in podocytes. |
| 1758 | 28052869 | In vitro, exposure of podocytes to Aldo enhanced NLRP3, caspase-1, and IL-18 expressions in dose- and time-dependent manners, indicating an activation of NLRP3 inflammasome, which was significantly blocked by the mineralocorticoid receptor antagonist eplerenone or the antioxidant N-acetylcysteine. |
| 1759 | 28052869 | Silencing NLRP3 by a siRNA approach strikingly attenuated Aldo-induced podocyte apoptosis and nephrin protein downregulation in line with the blockade of caspase-1 and IL-18. |
| 1760 | 28052869 | In vivo, since day 5 of Aldo infusion, NLRP3 inflammasome activation and podocyte injury evidenced by nephrin reduction occurred concurrently. |
| 1761 | 28052869 | In the mice with NLRP3 gene deletion, Aldo-induced downregulation of nephrin and podocin, podocyte foot processes, and albuminuria was remarkably improved, indicating an amelioration of podocyte injury. |
| 1762 | 28052869 | Finally, we observed a striking induction of NLRP3 in glomeruli and renal tubules in line with an enhanced urinary IL-18 output in nephrotic syndrome patients with minimal change disease or focal segmental glomerular sclerosis. |
| 1763 | 28117080 | Most often this occurred in the three most common SRNS-associated genes: NPHS1, NPHS2, and WT1 but also in 14 other genes. |
| 1764 | 28117080 | The genotype did not always correlate with expected phenotype since mutations in OCRL, COL4A3, and DGKE associated with specific syndromes were detected in patients with isolated renal disease. |
| 1765 | 28187984 | Last, we compared Cre efficiency in a disease model by mating Nphs2pod.T2A.ciCre.T2A.mTomato/wild-type and hNphs2.Cre mice to Phb2fl/fl mice. |
| 1766 | 28187984 | The podocyte-specific Phb2 knockout by Nphs2pod.T2A.ciCre.T2A.mTomato/wild-type mice resulted in an aggravated glomerular injury as compared to a podocyte-specific Phb2 gene deletion triggered by hNphs2.Cre. |
| 1767 | 28187984 | Last, we compared Cre efficiency in a disease model by mating Nphs2pod.T2A.ciCre.T2A.mTomato/wild-type and hNphs2.Cre mice to Phb2fl/fl mice. |
| 1768 | 28187984 | The podocyte-specific Phb2 knockout by Nphs2pod.T2A.ciCre.T2A.mTomato/wild-type mice resulted in an aggravated glomerular injury as compared to a podocyte-specific Phb2 gene deletion triggered by hNphs2.Cre. |
| 1769 | 28193546 | Contribution of guanine nucleotide exchange factor Vav2 to NLRP3 inflammasome activation in mouse podocytes during hyperhomocysteinemia. |
| 1770 | 28193546 | NADPH oxidase (NOX)-derived reactive oxygen species (ROS) have been demonstrated to mediate the activation of NOD-like receptor protein 3 (NLRP3) inflammasomes in podocytes in response to elevated levels of homocysteine (Hcys). |
| 1771 | 28193546 | The present study tested whether the guanine nucleotide exchange factor Vav2 mediates Rac1-mediated NOX activation in response to elevated Hcys leading to NLRP3 inflammasome activation in podocytes and consequent glomerular injury. |
| 1772 | 28193546 | In a mouse model of hyperhomocysteinemia (hHcys), we found that mice with hHcys (on the FF diet) or oncoVav2 (a constitutively active form of Vav2) transfection in the kidney exhibited increased colocalization of NLRP3 with apoptosis-associated speck-like protein (ASC) or caspase-1 and elevated IL-1β levels in glomeruli, indicating the formation and activation of the NLRP3 inflammasome. |
| 1773 | 28193546 | Furthermore, Vav2 shRNA prevented Hcys-induced podocyte damage as shown by restoring Hcys-impaired VEGF secretion and podocin production. |
| 1774 | 28193546 | This inhibitory action of Vav2 shRNA on Hcys-induced podocyte injury was associated with reduction of Rac1 activity and ROS production. |
| 1775 | 28193546 | These results suggest that elevated Hcys levels activate Vav2 and thereby increase NOX activity leading to ROS production, which triggers NLRP3 inflammasome activation, podocyte dysfunction and glomerular injury. |
| 1776 | 28223138 | Foxc1 and Foxc2 are necessary to maintain glomerular podocytes. |
| 1777 | 28223138 | Foxc1 and Foxc2 (Foxc1/2) are transcription factors involved in many biological processes. |
| 1778 | 28223138 | Comparison of gene expression profiles revealed that Foxc1/2 maintain expression of genes necessary for podocyte function such as podocin and Cxcl12. |
| 1779 | 28228401 | Wolf-Hirschhorn syndrome candidate 1-like 1 epigenetically regulates nephrin gene expression. |
| 1780 | 28228401 | Here, we show that Wolf-Hirschhorn syndrome candidate 1-like 1 long form (WHSC1L1-L) is a novel epigenetic modifier of nephrin gene regulation. |
| 1781 | 28228401 | Gene knockdown of WHSC1L1-L in primary cultured podocytes accelerated the transcription of nephrin but not CD2AP. |
| 1782 | 28228401 | An in vivo zebrafish study involving the injection of Whsc1l1 mRNA into embryos demonstrated an apparent reduction of nephrin mRNA but not podocin and CD2AP mRNA. |
| 1783 | 28228401 | Finally, nephrin mRNA was upregulated in the glomerulus at the early proteinuric stage of mouse nephrosis, which was associated with the reduction of WHSC1L1. |
| 1784 | 28266622 | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte. |
| 1785 | 28266622 | Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. |
| 1786 | 28266622 | Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin-Amphiphysin-Rvs (BAR) domain of SNX9. |
| 1787 | 28266622 | Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. |
| 1788 | 28266622 | In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| 1789 | 28266622 | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte. |
| 1790 | 28266622 | Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. |
| 1791 | 28266622 | Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin-Amphiphysin-Rvs (BAR) domain of SNX9. |
| 1792 | 28266622 | Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. |
| 1793 | 28266622 | In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| 1794 | 28266622 | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte. |
| 1795 | 28266622 | Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. |
| 1796 | 28266622 | Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin-Amphiphysin-Rvs (BAR) domain of SNX9. |
| 1797 | 28266622 | Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. |
| 1798 | 28266622 | In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| 1799 | 28266622 | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte. |
| 1800 | 28266622 | Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. |
| 1801 | 28266622 | Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin-Amphiphysin-Rvs (BAR) domain of SNX9. |
| 1802 | 28266622 | Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. |
| 1803 | 28266622 | In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| 1804 | 28266622 | Sorting Nexin 9 facilitates podocin endocytosis in the injured podocyte. |
| 1805 | 28266622 | Here we identified the protein sorting nexin 9 (SNX9) as a novel facilitator of podocin endocytosis in a yeast two-hybrid analysis. |
| 1806 | 28266622 | Our results revealed and confirmed that SNX9 interacts with podocin exclusively through the Bin-Amphiphysin-Rvs (BAR) domain of SNX9. |
| 1807 | 28266622 | Finally, an analysis of human glomerular disease biopsy samples demonstrated strong SNX9 expression and co-localization with podocin in samples representative of severe podocyte injury, such as IgA nephropathy with poor prognosis, membranous nephropathy and focal segmental glomerulosclerosis. |
| 1808 | 28266622 | In conclusion, we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of both nephropathy model mice and human patients with irreversible glomerular disease. |
| 1809 | 28277542 | MicroRNA-27a promotes podocyte injury via PPARγ-mediated β-catenin activation in diabetic nephropathy. |
| 1810 | 28277542 | MicroRNA-27a (miR-27a), peroxisome proliferator-activated receptor γ (PPARγ) and β-catenin pathways have been involved in the pathogenesis of DN. |
| 1811 | 28277542 | We found that high glucose stimulated miR-27a expression, which, by negatively targeting PPARγ, activated β-catenin signaling as evidenced by upregulation of β-catenin target genes, snail1 and α-smooth muscle actin (α-SMA) and downregulation of podocyte-specific markers podocin and synaptopodin. |
| 1812 | 28320523 | Moreover, the expression of synaptopodin and zonula occludens (ZO)-1 in RA-treated podocytes increased along with Krüppel-like factor 15 (KLF15) expression. |
| 1813 | 28320523 | Confocal microscopy revealed that RA increased the expression of cytoplasmic synaptopodin, which adopted a filamentous arrangement, and junctional ZO-1 expression, which showed a zipper-like pattern. |
| 1814 | 28320523 | The FSS+RA group showed increased synaptopodin and ZO-1 expression with prominent spikes on the cell-cell interface. |
| 1815 | 28320523 | Consistent with these data, the mRNA expression levels of synaptopodin, podocin, WT-1 and ZO-1 were synergistically increased by FSS and RA treatment. |
| 1816 | 28329012 | Four CoRL reporters (GFP, YFP, RFP, CFP) were restricted to cells in the juxtaglomerular compartment (JGC) at baseline. |
| 1817 | 28329012 | Following abrupt podocyte depletion in experimental FSGS, all four CoRL reporters were detected in a subset of glomeruli at day 28, where they co-expressed de novo four podocyte proteins (podocin, nephrin, WT-1 and p57) and two glomerular parietal epithelial cell (PEC) proteins (claudin-1, PAX8). |
| 1818 | 28413908 | For podocytes, expression of nephrin, podocin, P-cadherin, and ZO-1 is downregulated, the slit diaphragm (SD) will be altered, and the actin cytoskeleton will be rearranged. |
| 1819 | 28413908 | Diabetes, especially hyperglycemia, has been demonstrated to incite podocyte EMT through several molecular mechanisms such as TGF-β/Smad classic pathway, Wnt/β-catenin signaling pathway, Integrins/integrin-linked kinase (ILK) signaling pathway, MAPKs signaling pathway, Jagged/Notch signaling pathway, and NF-κB signaling pathway. |
| 1820 | 28502979 | Chrysin treatment dose-dependently restored the increased Bax/Bcl-2 ratio, and suppressed Apaf-1 induction and the elevated cytochrome c release in high glucose-exposed renal podocytes. |
| 1821 | 28502979 | In addition, this compound improved the induction of slit diaphragm proteins podocin/nephrin in the diabetic glomeruli. |
| 1822 | 28560004 | Protein expressions of inflammation (IL-1β/MMP-9), oxidative stress (NOX-1/NOX-2/oxidized protein, angiotensin-II receptor), apoptosis (Bax, cleaved caspase-3/PARP), fibrosis (Smad3/TGF-β), and kidney injured (KIM-1/FSP-1) markers showed an identical pattern, whereas anti-fibrosis (Smad5/BMP-2) indices exhibited an opposite pattern compared to that of creatinine level among all groups (all p < 0.01). |
| 1823 | 28560004 | Cellular expressions of inflammation (CD14/CD68), DNA-damage (γ-H2AX, CD90/XRCC1) and proximal-renal tubule (KIM-1) biomarkers displayed an identical pattern, whereas podocyte-integrity markers (podocin/ZO-1/p-cadherin/synaptopodin) showed a pattern opposite to that of creatinine level among all groups (all p < 0.001). |
| 1824 | 28583549 | Glomerular mRNA expression profiling showed down-regulations of podocyte-related genes (Wilms tumor 1, synaptopodin, nephrin, CD2-associated protein, and podocin) and of transforming growth factor-beta (a marker of fibrosis) in sirolimus-treated mice. |
| 1825 | 28583549 | In addition, expressions of the antiapoptotic genes Bcl-2 and Bcl-xL were also down-regulated. |
| 1826 | 28629718 | Rare genetic forms of FSGS can be caused by mutations in TRPC6, which encodes a Ca2+-permeable cationic channel expressed in mesangial cells and podocytes; and NPHS2, which encodes podocin, a TRPC6-binding protein expressed in podocyte slit diaphragm domains. |
| 1827 | 28629718 | Here we observed that exposing immortalized mouse podocytes to serum or plasma from recurrent FSGS patients for 24h increased the steady-state cell-surface abundance of TRPC6, accompanied by an increase in currents through endogenous TRPC6 channels evoked by a hypoosmotic stretch stimulus. |
| 1828 | 28629718 | Most but not all of the recurrent FSGS plasma samples that we examined also caused a loss of podocin over a period of several hours. |
| 1829 | 28629718 | The loss of podocin was also seen following exposure to suPAR but not TNF. |
| 1830 | 28629718 | However, TNF increased the effects of suPAR on TRPC6 and podocin, and TNF and suPAR are required for the full effects of one of the recurrent FSGS plasma samples. |
| 1831 | 28629718 | The actions of FSGS plasma, suPAR and TNF on surface abundance of TRPC6 were blocked by cilengitide, an inhibitor of αvβ3-integrin signaling. |
| 1832 | 28629718 | These data suggest that primary FSGS is a heterogeneous condition mediated by multiple circulating factors, and support TRPC6 and αvβ3-integrin as potential therapeutic targets. |
| 1833 | 28629718 | Rare genetic forms of FSGS can be caused by mutations in TRPC6, which encodes a Ca2+-permeable cationic channel expressed in mesangial cells and podocytes; and NPHS2, which encodes podocin, a TRPC6-binding protein expressed in podocyte slit diaphragm domains. |
| 1834 | 28629718 | Here we observed that exposing immortalized mouse podocytes to serum or plasma from recurrent FSGS patients for 24h increased the steady-state cell-surface abundance of TRPC6, accompanied by an increase in currents through endogenous TRPC6 channels evoked by a hypoosmotic stretch stimulus. |
| 1835 | 28629718 | Most but not all of the recurrent FSGS plasma samples that we examined also caused a loss of podocin over a period of several hours. |
| 1836 | 28629718 | The loss of podocin was also seen following exposure to suPAR but not TNF. |
| 1837 | 28629718 | However, TNF increased the effects of suPAR on TRPC6 and podocin, and TNF and suPAR are required for the full effects of one of the recurrent FSGS plasma samples. |
| 1838 | 28629718 | The actions of FSGS plasma, suPAR and TNF on surface abundance of TRPC6 were blocked by cilengitide, an inhibitor of αvβ3-integrin signaling. |
| 1839 | 28629718 | These data suggest that primary FSGS is a heterogeneous condition mediated by multiple circulating factors, and support TRPC6 and αvβ3-integrin as potential therapeutic targets. |
| 1840 | 28629718 | Rare genetic forms of FSGS can be caused by mutations in TRPC6, which encodes a Ca2+-permeable cationic channel expressed in mesangial cells and podocytes; and NPHS2, which encodes podocin, a TRPC6-binding protein expressed in podocyte slit diaphragm domains. |
| 1841 | 28629718 | Here we observed that exposing immortalized mouse podocytes to serum or plasma from recurrent FSGS patients for 24h increased the steady-state cell-surface abundance of TRPC6, accompanied by an increase in currents through endogenous TRPC6 channels evoked by a hypoosmotic stretch stimulus. |
| 1842 | 28629718 | Most but not all of the recurrent FSGS plasma samples that we examined also caused a loss of podocin over a period of several hours. |
| 1843 | 28629718 | The loss of podocin was also seen following exposure to suPAR but not TNF. |
| 1844 | 28629718 | However, TNF increased the effects of suPAR on TRPC6 and podocin, and TNF and suPAR are required for the full effects of one of the recurrent FSGS plasma samples. |
| 1845 | 28629718 | The actions of FSGS plasma, suPAR and TNF on surface abundance of TRPC6 were blocked by cilengitide, an inhibitor of αvβ3-integrin signaling. |
| 1846 | 28629718 | These data suggest that primary FSGS is a heterogeneous condition mediated by multiple circulating factors, and support TRPC6 and αvβ3-integrin as potential therapeutic targets. |
| 1847 | 28629718 | Rare genetic forms of FSGS can be caused by mutations in TRPC6, which encodes a Ca2+-permeable cationic channel expressed in mesangial cells and podocytes; and NPHS2, which encodes podocin, a TRPC6-binding protein expressed in podocyte slit diaphragm domains. |
| 1848 | 28629718 | Here we observed that exposing immortalized mouse podocytes to serum or plasma from recurrent FSGS patients for 24h increased the steady-state cell-surface abundance of TRPC6, accompanied by an increase in currents through endogenous TRPC6 channels evoked by a hypoosmotic stretch stimulus. |
| 1849 | 28629718 | Most but not all of the recurrent FSGS plasma samples that we examined also caused a loss of podocin over a period of several hours. |
| 1850 | 28629718 | The loss of podocin was also seen following exposure to suPAR but not TNF. |
| 1851 | 28629718 | However, TNF increased the effects of suPAR on TRPC6 and podocin, and TNF and suPAR are required for the full effects of one of the recurrent FSGS plasma samples. |
| 1852 | 28629718 | The actions of FSGS plasma, suPAR and TNF on surface abundance of TRPC6 were blocked by cilengitide, an inhibitor of αvβ3-integrin signaling. |
| 1853 | 28629718 | These data suggest that primary FSGS is a heterogeneous condition mediated by multiple circulating factors, and support TRPC6 and αvβ3-integrin as potential therapeutic targets. |
| 1854 | 28642201 | An elevated level of Nphs2 protein and reduced caspase 3 level indicated the preservation of podocytes and inhibition of cell apoptosis after CoQ10-lip+UTMD treatment. |
| 1855 | 28642201 | The molecular mechanism was associated with the upregulation of Bcl-2 and the downregulation of Bax. |
| 1856 | 28674043 | In FSGS-SCID mice, human Muse cells preferentially integrated into the damaged glomeruli and spontaneously differentiated into cells expressing markers of podocytes (podocin; 31%), mesangial cells (megsin; 13%), and endothelial cells (CD31; 41%) without fusing to the host cells; attenuated glomerular sclerosis and interstitial fibrosis; and induced the recovery of creatinine clearance at 7 weeks. |
| 1857 | 28724775 | We applied a novel proteomics technology that enables proteome-wide identification, mapping, and quantification of protein N-termini to comprehensively characterize cleaved podocyte proteins in the glomerulus in vivo We found evidence that defined proteolytic cleavage results in various proteoforms of important podocyte proteins, including those of podocin, nephrin, neph1, α-actinin-4, and vimentin. |
| 1858 | 28729288 | Renal histologic expression of the podocyte-specific protein, nephrin, but not podocin, is reduced in preeclamptic compared with normotensive pregnancies. |
| 1859 | 28729288 | Plasma measurements included HbF concentrations and concentrations of the endogenous chelators haptoglobin, hemopexin, and α1- microglobulin. |
| 1860 | 28729288 | Compared with urine from women with normotensive pregnancies, urine from women with preeclamptic pregnancies contained a high ratio of podocin-positive to nephrin-positive urinary EVs (podocin+ EVs-to-nephrin+ EVs ratio) and increased nephrinuria, both of which correlated with proteinuria. |
| 1861 | 28729288 | Plasma levels of hemopexin, which were decreased in women with preeclampsia, negatively correlated with proteinuria, urinary podocin+ EVs-to-nephrin+ EVs ratio, and nephrinuria. |
| 1862 | 28729288 | Furthermore, renal injury in preeclampsia associated with an elevated urinary podocin+ EVs-to-nephrin+ EVs ratio and may be mediated by prolonged exposure to cellfree HbF. |
| 1863 | 28729288 | Renal histologic expression of the podocyte-specific protein, nephrin, but not podocin, is reduced in preeclamptic compared with normotensive pregnancies. |
| 1864 | 28729288 | Plasma measurements included HbF concentrations and concentrations of the endogenous chelators haptoglobin, hemopexin, and α1- microglobulin. |
| 1865 | 28729288 | Compared with urine from women with normotensive pregnancies, urine from women with preeclamptic pregnancies contained a high ratio of podocin-positive to nephrin-positive urinary EVs (podocin+ EVs-to-nephrin+ EVs ratio) and increased nephrinuria, both of which correlated with proteinuria. |
| 1866 | 28729288 | Plasma levels of hemopexin, which were decreased in women with preeclampsia, negatively correlated with proteinuria, urinary podocin+ EVs-to-nephrin+ EVs ratio, and nephrinuria. |
| 1867 | 28729288 | Furthermore, renal injury in preeclampsia associated with an elevated urinary podocin+ EVs-to-nephrin+ EVs ratio and may be mediated by prolonged exposure to cellfree HbF. |
| 1868 | 28729288 | Renal histologic expression of the podocyte-specific protein, nephrin, but not podocin, is reduced in preeclamptic compared with normotensive pregnancies. |
| 1869 | 28729288 | Plasma measurements included HbF concentrations and concentrations of the endogenous chelators haptoglobin, hemopexin, and α1- microglobulin. |
| 1870 | 28729288 | Compared with urine from women with normotensive pregnancies, urine from women with preeclamptic pregnancies contained a high ratio of podocin-positive to nephrin-positive urinary EVs (podocin+ EVs-to-nephrin+ EVs ratio) and increased nephrinuria, both of which correlated with proteinuria. |
| 1871 | 28729288 | Plasma levels of hemopexin, which were decreased in women with preeclampsia, negatively correlated with proteinuria, urinary podocin+ EVs-to-nephrin+ EVs ratio, and nephrinuria. |
| 1872 | 28729288 | Furthermore, renal injury in preeclampsia associated with an elevated urinary podocin+ EVs-to-nephrin+ EVs ratio and may be mediated by prolonged exposure to cellfree HbF. |
| 1873 | 28729288 | Renal histologic expression of the podocyte-specific protein, nephrin, but not podocin, is reduced in preeclamptic compared with normotensive pregnancies. |
| 1874 | 28729288 | Plasma measurements included HbF concentrations and concentrations of the endogenous chelators haptoglobin, hemopexin, and α1- microglobulin. |
| 1875 | 28729288 | Compared with urine from women with normotensive pregnancies, urine from women with preeclamptic pregnancies contained a high ratio of podocin-positive to nephrin-positive urinary EVs (podocin+ EVs-to-nephrin+ EVs ratio) and increased nephrinuria, both of which correlated with proteinuria. |
| 1876 | 28729288 | Plasma levels of hemopexin, which were decreased in women with preeclampsia, negatively correlated with proteinuria, urinary podocin+ EVs-to-nephrin+ EVs ratio, and nephrinuria. |
| 1877 | 28729288 | Furthermore, renal injury in preeclampsia associated with an elevated urinary podocin+ EVs-to-nephrin+ EVs ratio and may be mediated by prolonged exposure to cellfree HbF. |
| 1878 | 28759006 | To explore the significance of Sall1 in differentiated podocytes, we investigated podocyte-specific Sall1-deficient mice (Sall1 KOp°d°/p°d°) using a podocin-Cre/loxP system and siRNA Sall1 knockdown (Sall1 KD) podocytes. |
| 1879 | 28759006 | Differentiated Sall1 KD podocytes showed a loss of synaptopodin, suppressed stress fiber formation, and, ultimately, impaired directed cell migration. |
| 1880 | 28759006 | These results indicated that Sall1 has a protective role in podocytes; thus, we investigated the endoplasmic reticulum stress marker GRP78. |
| 1881 | 28759006 | GRP78 expression was higher in ADR-treated Sall1 KOp°d°/p°d° mice than in control mice. |
| 1882 | 28759006 | Sall1 appeared to influence the expression of GRP78 in injured podocytes. |
| 1883 | 28843828 | The renal contents of advanced glycation end-products, interleukin-10, tissue growth factor-β, nuclear factor (NF)-κB and Ras-related C3 botulinum toxin substrate 1 (Rac 1) were decreased. |
| 1884 | 28843828 | Renal nephrin and podocin contents were increased and their mRNA expressions were replenished in vinpocetine-treated rats. |
| 1885 | 28843828 | This beneficial effect could be attributed to its antioxidant and antihyperglycemic effects parallel to its ability to inhibit NF-κB which eventually modulated cytokines production as well as nephrin and podocin proteins expression. |
| 1886 | 28843828 | The renal contents of advanced glycation end-products, interleukin-10, tissue growth factor-β, nuclear factor (NF)-κB and Ras-related C3 botulinum toxin substrate 1 (Rac 1) were decreased. |
| 1887 | 28843828 | Renal nephrin and podocin contents were increased and their mRNA expressions were replenished in vinpocetine-treated rats. |
| 1888 | 28843828 | This beneficial effect could be attributed to its antioxidant and antihyperglycemic effects parallel to its ability to inhibit NF-κB which eventually modulated cytokines production as well as nephrin and podocin proteins expression. |
| 1889 | 28849106 | Advanced glycation end products induce the apoptosis of and inflammation in mouse podocytes through CXCL9-mediated JAK2/STAT3 pathway activation. |
| 1890 | 28849106 | Based on an in vitro model of mouse podocyte injury, AGEs decreased the proliferation of podocytes and increased the expression of CXCL9 and C-X-C motif chemokine receptor 3 (CXCR3), and promoted the activation of signal transducer and activator of transcription 3 (STAT3). |
| 1891 | 28849106 | Moreover, the levels of inflammatory factors, such as tumor necrosis factor (TNF)‑α and interleukin (IL)‑6 were also decreased in the podoyctes transfected with siRNA-CXCL9, accompanied by the increased expression of nephrin and podocin, and decreased levels of Bax/Bcl-2 and activated caspase-3. |
| 1892 | 28849106 | The knockdown of CXCL9 also led to the inactivation of the Janus kinase 2 (JAK2)/STAT3 pathway. |
| 1893 | 28849106 | On the whole, and to the best of our knowledge, this study demonstrates for the first time that AGEs exert pro-apoptotic and pro-inflammatory effects in mouse podoyctes through the CXCL9-mediated activation of the JAK2/STAT3 pathway. |
| 1894 | 28852936 | Subsequently, thus-obtained Osr1+ cells were induced further with activin-A (10 ng/ml), RA (10 ng/ml), BMP-7 (2.5 ng/ml), EGF (30 ng/ml) and bFGF (30 ng/ml) for 9 days. |
| 1895 | 28852936 | Consequently, differentiated cells were immunopositive for anti-podocin, anti-synaptopodin and anti-GLEPP1 monoclonal antibodies. |
| 1896 | 28852936 | These cells showed expression of early podocyte markers PAX2 and Wt1 at day 3 followed by day 6 and mature podocyte markers NPHS1, SULT1B1, NPHS2 and Synaptopodin at day 9. |
| 1897 | 28852936 | Subsequently, thus-obtained Osr1+ cells were induced further with activin-A (10 ng/ml), RA (10 ng/ml), BMP-7 (2.5 ng/ml), EGF (30 ng/ml) and bFGF (30 ng/ml) for 9 days. |
| 1898 | 28852936 | Consequently, differentiated cells were immunopositive for anti-podocin, anti-synaptopodin and anti-GLEPP1 monoclonal antibodies. |
| 1899 | 28852936 | These cells showed expression of early podocyte markers PAX2 and Wt1 at day 3 followed by day 6 and mature podocyte markers NPHS1, SULT1B1, NPHS2 and Synaptopodin at day 9. |
| 1900 | 28879567 | mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis. |
| 1901 | 28879567 | Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis. |
| 1902 | 28879567 | In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin. |
| 1903 | 28879567 | In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment. |
| 1904 | 28879567 | By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction. |
| 1905 | 28879567 | Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade. |
| 1906 | 28879567 | Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction. |
| 1907 | 28879567 | More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines. |
| 1908 | 28879567 | Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis. |
| 1909 | 28879567 | Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy. |
| 1910 | 28879567 | mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis. |
| 1911 | 28879567 | Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis. |
| 1912 | 28879567 | In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin. |
| 1913 | 28879567 | In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment. |
| 1914 | 28879567 | By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction. |
| 1915 | 28879567 | Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade. |
| 1916 | 28879567 | Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction. |
| 1917 | 28879567 | More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines. |
| 1918 | 28879567 | Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis. |
| 1919 | 28879567 | Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy. |
| 1920 | 28879567 | mPGES-1-derived prostaglandin E2 stimulates Stat3 to promote podocyte apoptosis. |
| 1921 | 28879567 | Here we studied the role of mPGES-1/PGE2 cascade in activating Stat3 signaling and the contribution of Stat3 in PGE2- and Adr-induced podocyte apoptosis. |
| 1922 | 28879567 | In murine podocytes, PGE2 dose- and time-dependently increased the phosphorylation of Stat3 in line with the enhanced cell apoptosis and reduced podocyte protein podocin. |
| 1923 | 28879567 | In agreement with the increased Stat3 phosphorylation, Stat3-derived cytokines including IL-6, IL-17, MCP-1, and ICAM-1 were significantly upregulated following PGE2 treatment. |
| 1924 | 28879567 | By application of a specific Stat3 inhibitor S3I-201, PGE2-induced podocyte apoptosis was largely abolished in parallel with a blockade of podocin reduction. |
| 1925 | 28879567 | Next, we observed that Adr treatment also enhanced p-Stat3 and activated mPGES-1/PGE2 cascade. |
| 1926 | 28879567 | Blockade of Stat3 by S3I-201 significantly ameliorated Adr-induced cell apoptosis and podocin reduction. |
| 1927 | 28879567 | More interestingly, silencing mPGES-1 in podocytes by mPGES-1 siRNA blocked Adr-induced increments of Stat-3 phosphorylation, PGE2 production, and Stat3-derived inflammatory cytokines. |
| 1928 | 28879567 | Taken together, this study suggested that mPGES-1-derived PGE2 could activate Stat3 signaling to promote podocyte apoptosis. |
| 1929 | 28879567 | Targeting mPGES-1/PGE2/Stat3 signaling might be a potential strategy for the treatment of podocytopathy. |
| 1930 | 28905451 | Here, we show that hPSC-podocytes phenocopy mammalian podocytes at the capillary loop stage (CLS), recapitulating key features of ultrastructure, gene expression, and mutant phenotype. hPSC-podocytes in vitro progressively establish junction-rich basal membranes (nephrin+ podocin+ ZO-1+ ) and microvillus-rich apical membranes (podocalyxin+ ), similar to CLS podocytes in vivo. |
| 1931 | 28935820 | Serum- and glucocorticoid-inducible kinase 3 (SGK3) is a downstream mediator of PI3K, which is essential for maintaining the functional integrity of podocytes. |
| 1932 | 28935820 | Short hairpin RNA (shRNA)-mediated knockdown of SGK3 also reduced podocin expression in the absence of PAN. |
| 1933 | 28935820 | Consistent with a role for SGK3 in the ADR effect, SGK3 knockout (KO) mice had markedly reduced kidney podocin expression and significantly elevated proteinuria compared with wild-type mice. |
| 1934 | 28935820 | Serum- and glucocorticoid-inducible kinase 3 (SGK3) is a downstream mediator of PI3K, which is essential for maintaining the functional integrity of podocytes. |
| 1935 | 28935820 | Short hairpin RNA (shRNA)-mediated knockdown of SGK3 also reduced podocin expression in the absence of PAN. |
| 1936 | 28935820 | Consistent with a role for SGK3 in the ADR effect, SGK3 knockout (KO) mice had markedly reduced kidney podocin expression and significantly elevated proteinuria compared with wild-type mice. |
| 1937 | 29038743 | Here, we demonstrate an efficient (> 90%) and chemically defined method for directing the differentiation of human induced pluripotent stem (hiPS) cells into podocytes that express markers of the mature phenotype (nephrin+, WT1+, podocin+, Pax2-) and that exhibit primary and secondary foot processes. |
| 1938 | 29038743 | We also show that the hiPS-cell-derived podocytes produce glomerular basement-membrane collagen and recapitulate the natural tissue/tissue interface of the glomerulus, as well as the differential clearance of albumin and inulin, when co-cultured with human glomerular endothelial cells in an organ-on-a-chip microfluidic device. |
| 1939 | 29038896 | Compared with the control (C57 or BKS), ATF3 expression was elevated in animal model of proteinuria (LPS-treated C57 mice) and the model of diabetic nephropathy (db/db mice). |
| 1940 | 29038896 | Overexpression of ATF3 increased podocyte apoptosis and decreased expression of podocin, the cell marker of podocyte; in contrast, ATF3-small interfering RNA knockdown reduced podocyte apoptosis and increased podocin expression. |
| 1941 | 29038896 | ATF3 directly modulates the regulation of NFATc1 gene promoter activity and alters the expression of Wnt6 and Fzd9, direct target genes of NFATc1 signaling. |
| 1942 | 29038896 | The ATF3 binding site of NFATc1 gene promoter is located at the region 671-775 base pairs upstream of the transcription start site. |
| 1943 | 29070572 | Fasting blood glucose and insulin and the expression of podocin, nephrin, phosphoinositide 3-kinase (PI3K), glucose transporter type (Glut4), and microtubule-associated protein 1A/1B-light chain 3 (LC3) were assayed. |
| 1944 | 29070572 | The decreased translocation of Glut4 to the plasma membrane and excess autophagy seen in mice fed a high-fat diet and in PA-treated cultured podocytes were attenuated by GLP-1. |
| 1945 | 29070572 | GLP-1 restored insulin sensitivity and ameliorated renal injury by decreasing the level of autophagy. |
| 1946 | 29110957 | The kidney expresses protease-activated receptor-1 (PAR-1). |
| 1947 | 29110957 | PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood. |
| 1948 | 29110957 | Pathological analysis showed that Q94 treatment significantly attenuated periodic acid-Schiff and desmin staining, indicators of podocyte injury, and also decreased glomerular levels of podocin and nephrin. |
| 1949 | 29110957 | In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes. |
| 1950 | 29115406 | Tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) has been demonstrated to mediate the activation of nuclear factor-κB (NF-κB), which has been implicated in the pathogenesis of chronic kidney disease (CKD). |
| 1951 | 29115406 | The NF-κB inhibitor, caffeic acid phenethyl ester (CAPE), mimicked the protective effects of BBR, as evidenced by the increased expression of nephrin and podocin, and the decreased the expression of caspase-3 and the ratio of Bax/Bcl-2. |
| 1952 | 29138824 | However, FSGS does not result exclusively from podocyte‑associated genes, however also from other genes including collagen IV‑associated genes. |
| 1953 | 29138824 | Patients who carry the collagen type IVA3 chain (COL4A3) or COL4A4 mutations usually exhibit Alport Syndrome (AS), thin basement membrane neuropathy or familial hematuria (FH). |
| 1954 | 29138824 | Genomic DNA of the siblings affected by FH with biopsy‑proven FSGS was analyzed, and their father was screened for 18 gene mutations associated with FSGS [nephrin, podocin, CD2 associated protein, phospholipase C ε, actinin α 4, transient receptor potential cation channel subfamily C member 6, inverted formin, FH2 and WH2 domain containing, Wilms tumor 1, LIM homeobox transcription factor 1 β, laminin subunit β 2, laminin subunit β 3, galactosida α, integrin subunit β 4, scavenger receptor class B member 2, coenzyme Q2, decaprenyl diphosphate synthase subunit 2, mitochondrially encoded tRNA leucine 1 (UUA/G; TRNL1) and SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a like 1] using matrix‑assisted laser desorption/ionization time‑of‑flight mass spectrometry technology. |
| 1955 | 29138824 | Using mass array technology, a TRNL1 missense homozygous mutation (m. 3290T>C) was identified in the probands diagnosed with FH and manifested as FSGS on biopsy. |
| 1956 | 29138824 | In the present study, a mutation in TRNL1 (m. 3290T>C) was identified, which was the first reported variant associated with FSGS. |
| 1957 | 29138824 | The COL4A4 (c. 4195A>T) may co‑segregate with FSGS. |
| 1958 | 29175208 | A single nucleotide polymorphism (SNP) within the acetyl CoA carboxylase (ACC) β gene (ACACB), rs2268388, has been shown to be associated with susceptibility to development of proteinuria in patients with type 2 diabetes. |
| 1959 | 29175208 | In STZ-induced diabetic mice, ACACB-transgenic mice showed a significant increase in urinary albumin excretion, accompanied by decreased synaptopodin expression and podocin mislocalization in podocytes, compared with wild-type mice. |
| 1960 | 29175208 | In cultured murine podocytes, overexpression of ACACB significantly decreased synaptopodin expression and reorganized stress fibers under high glucose conditions, but not in normal glucose conditions. |
| 1961 | 29175208 | The decrease of synaptopodin expression and reorganized stress fibers observed in ACACB overexpressing cells cultured under high glucose conditions was reversed by a treatment of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR), activator of AMP-activated protein kinase (AMPK). |
| 1962 | 29244787 | These slits are covered by a number of surface proteins, such as nephrin, podocin, podocalyxin and CD2AP. |
| 1963 | 29246788 | Five-week-old rats were fed with high-fat diet for 18weeks to establish the ORG model, then the histological change of glomeruli, the foot process effacement of podocyte, the markers for podocyte injury (nephrin,podocin and WT1) and Cx43 expression in glomeruli were examined respectively. |
| 1964 | 29328453 | In the in vivo animal experiments, body weight, Lee's obesity index, abdominal fat index, urinary protein excretion, average glomerular diameter were significantly increased, the mRNA and protein expression of podocyte‑associated molecules including nephrin, podocin, podoplanin and podocalyxin were significantly reduced, and the Wnt/β‑catenin signaling pathway was activated in ORG model mice compared with the Control mice, whereas the administration of spironolactone significantly ameliorated these effects. |
| 1965 | 29335087 | Transient receptor potential cation channel 6 (TRPC6) is a member of the transient receptor superfamily encoded by the TRPC6 gene and is widely expressed in tissues and organs of the human body, especially in the glomerular podocytes. |
| 1966 | 29335087 | TRPC6 interacts with various slit diaphragm (SD) proteins including podocin, nephrin, ACTN4, and CD2AP to maintain the normal structure and function of glomerular podocytes. |
| 1967 | 29361670 | The inducible podocyte-specific PTEN knockin (PPKI) mice were generated by crossing newly created transgenic loxP-stop- loxP-PTEN mice with podocin-iCreERT2 mice. |
| 1968 | 29382718 | In addition, we demonstrate an enhanced interaction of podocinR138Q with calnexin as the mechanism of endoplasmic reticulum retention. |
| 1969 | 29382718 | Calnexin knockdown enriches the podocinR138Q non-glycosylated fraction, whereas preventing exit from the calnexin cycle increases the glycosylated fraction. |
| 1970 | 29382718 | Altogether, we propose a model in which hairpin podocinR138Q is rapidly degraded by the proteasome, whereas transmembrane podocinR138Q degradation is delayed due to entry into the calnexin cycle. |
| 1971 | 29382718 | In addition, we demonstrate an enhanced interaction of podocinR138Q with calnexin as the mechanism of endoplasmic reticulum retention. |
| 1972 | 29382718 | Calnexin knockdown enriches the podocinR138Q non-glycosylated fraction, whereas preventing exit from the calnexin cycle increases the glycosylated fraction. |
| 1973 | 29382718 | Altogether, we propose a model in which hairpin podocinR138Q is rapidly degraded by the proteasome, whereas transmembrane podocinR138Q degradation is delayed due to entry into the calnexin cycle. |
| 1974 | 29382718 | In addition, we demonstrate an enhanced interaction of podocinR138Q with calnexin as the mechanism of endoplasmic reticulum retention. |
| 1975 | 29382718 | Calnexin knockdown enriches the podocinR138Q non-glycosylated fraction, whereas preventing exit from the calnexin cycle increases the glycosylated fraction. |
| 1976 | 29382718 | Altogether, we propose a model in which hairpin podocinR138Q is rapidly degraded by the proteasome, whereas transmembrane podocinR138Q degradation is delayed due to entry into the calnexin cycle. |
| 1977 | 29446486 | Interleukin-17A participates in podocyte injury by inducing IL-1β secretion through ROS-NLRP3 inflammasome-caspase-1 pathway. |
| 1978 | 29446486 | Also, activity of caspase-1 and secretion of IL-1β increased in the presence of IL-17A. |
| 1979 | 29446486 | In addition, IL-17A disrupted podocyte morphology by decreasing expression of podocin and increasing expression of desmin. |
| 1980 | 29446486 | Taken together, the results suggest that IL-17A induces podocyte injury by activating the NLRP3 inflammasome and IL-1β secretion and contributes to disruption of the kidney's filtration system. |
| 1981 | 29518610 | To further demonstrate the protective effects of ZWT, we found that podocyte damage was markedly ameliorated with ZWT treatments in IgAN rats and LPS-induced podocyte injury model by suppressing the expressions of desmin, reducing podocyte apoptosis and augmenting nephrin and podocin levels. |
| 1982 | 29552824 | Secondly, the protein expression levels of the epithelial markers in podocytes such as nephrin and podocin, the mesenchymal markers such as desmin and collagen Ⅰ and the EMT-related mediators such as snail were detected respectively. |
| 1983 | 29552824 | The results indicated that, HG could cause the low protein expression levels of nephrin and podocin and the high protein expression levels of desmin, collagen Ⅰ and snail in podocytes, and inducing podocyte EMT. |
| 1984 | 29552824 | In addition, L-TP had no effect on the activation of podocyte proliferation, the co-treatment of L-TP and HG could significantly recover the protein expression levels of nephrin and podocin, inhibit the protein expression levels of desmin, collagen I and snail in podocytes, thus, further improving podocyte EMT. |
| 1985 | 29552824 | Secondly, the protein expression levels of the epithelial markers in podocytes such as nephrin and podocin, the mesenchymal markers such as desmin and collagen Ⅰ and the EMT-related mediators such as snail were detected respectively. |
| 1986 | 29552824 | The results indicated that, HG could cause the low protein expression levels of nephrin and podocin and the high protein expression levels of desmin, collagen Ⅰ and snail in podocytes, and inducing podocyte EMT. |
| 1987 | 29552824 | In addition, L-TP had no effect on the activation of podocyte proliferation, the co-treatment of L-TP and HG could significantly recover the protein expression levels of nephrin and podocin, inhibit the protein expression levels of desmin, collagen I and snail in podocytes, thus, further improving podocyte EMT. |
| 1988 | 29552824 | Secondly, the protein expression levels of the epithelial markers in podocytes such as nephrin and podocin, the mesenchymal markers such as desmin and collagen Ⅰ and the EMT-related mediators such as snail were detected respectively. |
| 1989 | 29552824 | The results indicated that, HG could cause the low protein expression levels of nephrin and podocin and the high protein expression levels of desmin, collagen Ⅰ and snail in podocytes, and inducing podocyte EMT. |
| 1990 | 29552824 | In addition, L-TP had no effect on the activation of podocyte proliferation, the co-treatment of L-TP and HG could significantly recover the protein expression levels of nephrin and podocin, inhibit the protein expression levels of desmin, collagen I and snail in podocytes, thus, further improving podocyte EMT. |
| 1991 | 29556761 | A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. |
| 1992 | 29572435 | RESULTS β-arrestin 1/2 expression levels of podocytes were up-regulated in high-glucose-induced podocytes. β-arrestin 1/2 overexpression inhibited the expression of nephrin and podocin protein. |
| 1993 | 29572435 | Up-regulated β-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. |
| 1994 | 29572435 | Wnt/b-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by β-arrestin 1/2 overexpression and high glucose. |
| 1995 | 29689364 | HbG induced marked proteinuria characterized in part by the loss of high molecular weight proteins, including albumin, immunoglobulin, and transferrin, at 4 and 12 h post-infusion that resolved by 72 h. |
| 1996 | 29689364 | This correlated with HbG-induced GFB alterations based on the reduced expression of specific markers of podocytes (podocin, nephrin, podocalyxin, and Wilms Tumor 1 protein) and endothelial cells (ETS-related gene and claudin-5). |
| 1997 | 29704630 | We also investigated the effect of NUP160 knockdown on the expression and localization of podocyte associated molecules, such as nephrin, podocin, CD2AP and α-actinin-4. |
| 1998 | 29704630 | The knockdown of NUP160 significantly inhibited the proliferation of podocytes by decreasing the expression of both cyclin D1 and CDK4, increasing the expression of p27, and inducing S phase arrest. |
| 1999 | 29704630 | The knockdown of NUP160 decreased the expression of nephrin, podocin and CD2AP in podocytes, and increased the expression of α-actinin-4. |
| 2000 | 29704630 | The knockdown of NUP160 also altered the subcellular localization of nephrin, podocin and CD2AP in podocytes. |
| 2001 | 29704630 | These results suggest that the knockdown of NUP160 impairs mouse podocytes, i.e. inhibiting cell proliferation, inducing apoptosis, autophagy and cell migration of mouse podocytes, and altering the expression and localization of podocyte associated molecules, including nephrin, podocin, CD2AP and α-actinin-4. |
| 2002 | 29704630 | We also investigated the effect of NUP160 knockdown on the expression and localization of podocyte associated molecules, such as nephrin, podocin, CD2AP and α-actinin-4. |
| 2003 | 29704630 | The knockdown of NUP160 significantly inhibited the proliferation of podocytes by decreasing the expression of both cyclin D1 and CDK4, increasing the expression of p27, and inducing S phase arrest. |
| 2004 | 29704630 | The knockdown of NUP160 decreased the expression of nephrin, podocin and CD2AP in podocytes, and increased the expression of α-actinin-4. |
| 2005 | 29704630 | The knockdown of NUP160 also altered the subcellular localization of nephrin, podocin and CD2AP in podocytes. |
| 2006 | 29704630 | These results suggest that the knockdown of NUP160 impairs mouse podocytes, i.e. inhibiting cell proliferation, inducing apoptosis, autophagy and cell migration of mouse podocytes, and altering the expression and localization of podocyte associated molecules, including nephrin, podocin, CD2AP and α-actinin-4. |
| 2007 | 29704630 | We also investigated the effect of NUP160 knockdown on the expression and localization of podocyte associated molecules, such as nephrin, podocin, CD2AP and α-actinin-4. |
| 2008 | 29704630 | The knockdown of NUP160 significantly inhibited the proliferation of podocytes by decreasing the expression of both cyclin D1 and CDK4, increasing the expression of p27, and inducing S phase arrest. |
| 2009 | 29704630 | The knockdown of NUP160 decreased the expression of nephrin, podocin and CD2AP in podocytes, and increased the expression of α-actinin-4. |
| 2010 | 29704630 | The knockdown of NUP160 also altered the subcellular localization of nephrin, podocin and CD2AP in podocytes. |
| 2011 | 29704630 | These results suggest that the knockdown of NUP160 impairs mouse podocytes, i.e. inhibiting cell proliferation, inducing apoptosis, autophagy and cell migration of mouse podocytes, and altering the expression and localization of podocyte associated molecules, including nephrin, podocin, CD2AP and α-actinin-4. |
| 2012 | 29704630 | We also investigated the effect of NUP160 knockdown on the expression and localization of podocyte associated molecules, such as nephrin, podocin, CD2AP and α-actinin-4. |
| 2013 | 29704630 | The knockdown of NUP160 significantly inhibited the proliferation of podocytes by decreasing the expression of both cyclin D1 and CDK4, increasing the expression of p27, and inducing S phase arrest. |
| 2014 | 29704630 | The knockdown of NUP160 decreased the expression of nephrin, podocin and CD2AP in podocytes, and increased the expression of α-actinin-4. |
| 2015 | 29704630 | The knockdown of NUP160 also altered the subcellular localization of nephrin, podocin and CD2AP in podocytes. |
| 2016 | 29704630 | These results suggest that the knockdown of NUP160 impairs mouse podocytes, i.e. inhibiting cell proliferation, inducing apoptosis, autophagy and cell migration of mouse podocytes, and altering the expression and localization of podocyte associated molecules, including nephrin, podocin, CD2AP and α-actinin-4. |
| 2017 | 29746568 | The protective effect of the EP2 receptor on TGF-β1 induced podocyte injury via the PI3K / Akt signaling pathway. |
| 2018 | 29746568 | Previous studies have shown that phosphoinositide 3-OH kinase (PI3K)/Akt is widespread in cells, and is vital for the regulation of cell proliferation, differentiation, apoptosis and metabolism. |
| 2019 | 29746568 | Meanwhile, expressions of nephrin, podocin and CD2AP mRNA and protein were dramatically downregulated, activated caspase-3 was increased, and activated PI3K/Akt activity were depressed. |
| 2020 | 29746568 | This causes the interaction of nephrin, podocin and CD2AP resulting the inhibition of apoptosis induced by activation of the PI3K / Akt signaling pathway. |
| 2021 | 29746568 | The protective effect of the EP2 receptor on TGF-β1 induced podocyte injury via the PI3K / Akt signaling pathway. |
| 2022 | 29746568 | Previous studies have shown that phosphoinositide 3-OH kinase (PI3K)/Akt is widespread in cells, and is vital for the regulation of cell proliferation, differentiation, apoptosis and metabolism. |
| 2023 | 29746568 | Meanwhile, expressions of nephrin, podocin and CD2AP mRNA and protein were dramatically downregulated, activated caspase-3 was increased, and activated PI3K/Akt activity were depressed. |
| 2024 | 29746568 | This causes the interaction of nephrin, podocin and CD2AP resulting the inhibition of apoptosis induced by activation of the PI3K / Akt signaling pathway. |
| 2025 | 29845208 | Notably, treatment with GLP‑1 attenuated HG‑induced increases in ROS production and podocyte apoptosis, which may occur via downregulation of the expression of caspase‑3 and caspase‑9, and increased expression of nephrin, podocin and SIRT1, as determined by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. |
| 2026 | 29931909 | [Effects of ferulic acid on the expressions of nephrin and podocin in podocytes of diabetic rats]. |
| 2027 | 29948786 | It ameliorated glomerular injury due to diabetes by increasing glomerular nephrin and synaptopodin expressions, mitigating renal integrin-linked kinase (ILK) levels, and lowering urinary albumin, collagen type IV, and podocin excretions. |
| 2028 | 29948786 | Additionally, the combination also alleviated indices of renal inflammation as revealed by decreased renal monocyte chemoattractant protein 1 (MCP-1) and chemokine (C-X-C motif) ligand 12 (CXCL12) expressions, F4/80-positive macrophages, glomerular TUNEL-positive cells, and urinary alpha-1-acid glycoprotein (AGP) levels. |
| 2029 | 29960864 | Using a quantitative polymerase chain reaction of the podocyte-specific molecules nephrin, podocin, and VEGF-A in the urine, we examined whether podocyturia is present in bevacizumab-treated cancer patients, and whether it relates to proteinuria and the cumulative dose of bevacizumab. |
| 2030 | 29960864 | Urinary podocin mRNA expression was undetectable in 59% of participants, urinary nephrin mRNA expression per mmol creatinine ranged from 0.0 to 5.3 and urinary VEGF-A mRNA expression from 0.0 to 2.7. |
| 2031 | 29960864 | Urinary nephrin mRNA expression did not correlate to the albumin-to-creatinine ratio or the cumulative dose of bevacizumab, whereas the latter correlated with the albumin-to-creatinine ratio (r = 0.77; P < .001). |
| 2032 | 29960864 | Using a quantitative polymerase chain reaction of the podocyte-specific molecules nephrin, podocin, and VEGF-A in the urine, we examined whether podocyturia is present in bevacizumab-treated cancer patients, and whether it relates to proteinuria and the cumulative dose of bevacizumab. |
| 2033 | 29960864 | Urinary podocin mRNA expression was undetectable in 59% of participants, urinary nephrin mRNA expression per mmol creatinine ranged from 0.0 to 5.3 and urinary VEGF-A mRNA expression from 0.0 to 2.7. |
| 2034 | 29960864 | Urinary nephrin mRNA expression did not correlate to the albumin-to-creatinine ratio or the cumulative dose of bevacizumab, whereas the latter correlated with the albumin-to-creatinine ratio (r = 0.77; P < .001). |
| 2035 | 29967295 | Consistently, the expression levels of nephrin and podocin proteins were significantly decreased in the G1- or G2-overexpressing cells despite the maintenance of their mRNA expressions levels. |
| 2036 | 29967295 | In contrast, the expression of the 78-kDa glucose-regulated protein ((GRP78), also known as the binding Ig protein, BiP) and the phosphorylation of the eukaryotic translation initiation factor 1 (eIF1) were significantly elevated in the G1/HPs and G2/HPs, suggesting a possible occurrence of ER stress in these cells. |
| 2037 | 29967295 | Furthermore, ER stress inhibitors not only restored nephrin protein expression, but also provided protection against necrosis in G1/HPs and G2/HPs, suggesting that APOL1 risk variants cause podocyte injury partly through enhancing ER stress. |
| 2038 | 29980767 | Further, immunopositive area of endothelial marker (CD34), podocyte functional molecules (Nephrin, Podocin, Synaptopodin, and Wilms' tumour 1 (WT1)), and vascular endothelial growth factor A (VEGF A) significantly decreased in the glomerulus of BXSB/MpJ-Yaa compared with BXSB at final stage. |
| 2039 | 29980767 | The indices of glomerular endothelial injuries (EF density and immunopositive area of CD34 and VEGF A) and podocyte injuries (PEP density and immunopositive area of podocyte functional molecules) were also significantly correlated with each other and with indices of autoimmune disease and renal dysfunction. |
| 2040 | 30019931 | Within glomeruli, RFP-labeled cells did not coexpress podocyte proteins (p57, synaptopodin, nephrin, or podocin) but did coexpress markers for mesangial (α8 integrin, PDGFβ receptor) and parietal epithelial cells (PAX8, src-suppressed C-kinase substrate). |
| 2041 | 30099615 | Mutations in nephrin (NPHS1), podocin (NPHS2), laminin β2 (LAMB2), and α-actinin-4 (ACTN4) have been shown to induce ER stress in HEK293 cells and podocytes in hereditary nephrotic syndromes; various founder mutations in collagen IV α chains (COL4A) have been demonstrated to activate podocyte ER stress in collagen IV nephropathies; and mutations in uromodulin (UMOD) have been reported to trigger tubular ER stress in autosomal dominant tubulointerstitial kidney disease. |
| 2042 | 30099615 | Recently, we have identified mesencephalic astrocyte-derived neurotrophic factor (MANF) and cysteine-rich with EGF-like domains 2 (CRELD2) as urinary ER stress biomarkers in ER stress-mediated kidney diseases. |
| 2043 | 30133147 | Therefore, we measured urinary mRNA levels of podocyte genes NPHS1, NPHS2, PODXL and BDNF, KIM-1, CTSL by qRT-PCR of 120 CKD patients. |
| 2044 | 30133147 | We showed a strong correlation between BDNF and the kidney injury marker KIM-1, which were also correlated with NPHS1, suggesting podocytes as a contributing source. |
| 2045 | 30133147 | An inhibition of the BDNF receptor TrkB resulted in enhanced podocyte dedifferentiation. |
| 2046 | 30133147 | We demonstrated that BDNF is essential for glomerular development, morphology and function and the expression of BDNF and KIM-1 is highly correlated in urine cells of CKD patients. |
| 2047 | 30210570 | And then, blood glucose, urine protein, renal index, renal microstructural (HE/PAS staining), inflammatory factors (IL-β, TNF-α, IL-6), and protein/mRNA expression related to the function of podocyte (CD2AP and Podocin) in DN rats were investigated after the oral administration of EZF. |
| 2048 | 30210570 | The expressions of Podocin and CD2AP protein/mRNA were increased (P < 0. 05). |
| 2049 | 30210570 | All the results proved that EZF repaired glomerular mesangial matrix, protected renal tubule, and improved renal function in DN rats by upregulating the expression of Podocin and CD2AP protein/mRNA in podocytes. |
| 2050 | 30210570 | And then, blood glucose, urine protein, renal index, renal microstructural (HE/PAS staining), inflammatory factors (IL-β, TNF-α, IL-6), and protein/mRNA expression related to the function of podocyte (CD2AP and Podocin) in DN rats were investigated after the oral administration of EZF. |
| 2051 | 30210570 | The expressions of Podocin and CD2AP protein/mRNA were increased (P < 0. 05). |
| 2052 | 30210570 | All the results proved that EZF repaired glomerular mesangial matrix, protected renal tubule, and improved renal function in DN rats by upregulating the expression of Podocin and CD2AP protein/mRNA in podocytes. |
| 2053 | 30210570 | And then, blood glucose, urine protein, renal index, renal microstructural (HE/PAS staining), inflammatory factors (IL-β, TNF-α, IL-6), and protein/mRNA expression related to the function of podocyte (CD2AP and Podocin) in DN rats were investigated after the oral administration of EZF. |
| 2054 | 30210570 | The expressions of Podocin and CD2AP protein/mRNA were increased (P < 0. 05). |
| 2055 | 30210570 | All the results proved that EZF repaired glomerular mesangial matrix, protected renal tubule, and improved renal function in DN rats by upregulating the expression of Podocin and CD2AP protein/mRNA in podocytes. |
| 2056 | 30222766 | Conditionally immortalized human podocytes served as reference controls. iPSC-derived podocyte-like cells showed a typical podocyte-specific morphology and distinct expression of podocyte markers synaptopodin, podocin, nephrin and WT-1 after 10 days of differentiation as assessed by immunofluorescence staining or Western blot analysis. qPCR results showed a downregulation of pluripotency markers Oct4 and Sox-2 and a 9-fold upregulation of the podocyte marker synaptopodin during the time course of differentiation. |
| 2057 | 30255020 | In this review, we will focus on slit diaphragm proteins such as nephrin, podocin, TRPC6/5, as well as cytoskeletal proteins Rho/small GTPases and synaptopodin and their respective roles in participating in the pathogenesis of proteinuric kidney diseases. |
| 2058 | 30359671 | The adult offspring kidneys in the PDE group displayed glomerulosclerosis, elevated levels of serum creatinine and urine protein, ultrastructural damage of podocytes, the reduced expression levels of podocyte marker genes, nephrin and podocin. |
| 2059 | 30359671 | The histone 3 lysine 9 acetylation (H3K9ac) level in the promoter of renal angiotensin II receptor type 2 (AT2R) and its expression were reduced, whereas the angiotensin II receptor type 1a (AT1aR)/AT2R expression ratio was increased. |
| 2060 | 30359671 | The fetal kidneys in the PDE group displayed an enlarged Bowman's space and a shrunken glomerular tuft, a reduced cortex width and an increase in the nephrogenic zone/cortical zone ratio, reduced the expression level of glial-cell-line derived neurotrophic factor/c-Ret tyrosine kinase receptor (GDNF/c-Ret) signal pathway and podocyte marker genes. |
| 2061 | 30359671 | Overexpression of AT2R reversed the inhibited expression of GDNF/c-Ret and podocin/nephrin induced by dexamethasone, and glucocorticoids receptor antagonist abolished the decreased H3K9ac level and gene expression of AT2R. |
| 2062 | 30359671 | The adult offspring kidneys in the PDE group displayed glomerulosclerosis, elevated levels of serum creatinine and urine protein, ultrastructural damage of podocytes, the reduced expression levels of podocyte marker genes, nephrin and podocin. |
| 2063 | 30359671 | The histone 3 lysine 9 acetylation (H3K9ac) level in the promoter of renal angiotensin II receptor type 2 (AT2R) and its expression were reduced, whereas the angiotensin II receptor type 1a (AT1aR)/AT2R expression ratio was increased. |
| 2064 | 30359671 | The fetal kidneys in the PDE group displayed an enlarged Bowman's space and a shrunken glomerular tuft, a reduced cortex width and an increase in the nephrogenic zone/cortical zone ratio, reduced the expression level of glial-cell-line derived neurotrophic factor/c-Ret tyrosine kinase receptor (GDNF/c-Ret) signal pathway and podocyte marker genes. |
| 2065 | 30359671 | Overexpression of AT2R reversed the inhibited expression of GDNF/c-Ret and podocin/nephrin induced by dexamethasone, and glucocorticoids receptor antagonist abolished the decreased H3K9ac level and gene expression of AT2R. |
| 2066 | 30379099 | We performed polysome analysis of intact and injured podocytes utilizing the NEP25 and RiboTag transgenic mice, in which a hemagglutinin tag is attached to ribosomal protein L22 selectively in podocytes. |
| 2067 | 30379099 | Compared with glomerular cells, 353 genes were highly expressed and enriched in podocytes; these included important podocyte genes and also heretofore uncharacterized genes, such as Dach1 and Foxd2. |
| 2068 | 30379099 | MafF and Egr-1, which structurally have the potential to antagonize MafB and WT1, respectively, were rapidly and markedly increased in injured podocytes before MafB and WT1 were decreased. |
| 2069 | 30379099 | We demonstrated that Maff and Egr1 knockdown increased the MafB targets Nphs2 and Ptpro and the WT1 targets Ptpro, Nxph3, and Sulf1, respectively. |
| 2070 | 30379099 | This indicates that upregulated MafF and Egr-1 may promote deterioration of podocytes by antagonizing MafB and WT1. |
| 2071 | 30387200 | A sustained increase in hypoxia-inducible factor 1α (HIF1α) is a major adaptive stimulus to the hypoxic conditions. |
| 2072 | 30387200 | The elevated HIF1α expression is concurrence with diminished expression of nephrin and podocin, podocyte foot-processes effacement, and significant proteinuria. |
| 2073 | 30387200 | Elevation in expression of HIF1α is in concomitance with loss of nephrin and podocin in patients with diabetic nephropathy and chronic kidney disease. |
| 2074 | 30387200 | A sustained increase in hypoxia-inducible factor 1α (HIF1α) is a major adaptive stimulus to the hypoxic conditions. |
| 2075 | 30387200 | The elevated HIF1α expression is concurrence with diminished expression of nephrin and podocin, podocyte foot-processes effacement, and significant proteinuria. |
| 2076 | 30387200 | Elevation in expression of HIF1α is in concomitance with loss of nephrin and podocin in patients with diabetic nephropathy and chronic kidney disease. |
| 2077 | 30472210 | Dual staining of PCX+podo was positive for Glepp 1 (50%), whereas none of PCX+podo were positive for nephrin, podocin, leukocyte, or parietal epithelial cell markers (cytokeratin 8), annexin V, cleaved caspase-3, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. |
| 2078 | 30496699 | Most of these cells exhibited endothelial phenotypes, being negative for several markers, including podocin (a maker of podocyte), α8 integrin (mesangial cell), CD68, and F4/80 (macrophage). |
| 2079 | 30545560 | Epidermal growth factor receptor and podocin predict nephropathy progression in type 2 diabetic patients through interaction with the autophagy influencer ULK-1. |
| 2080 | 30691124 | We identified cases of FSGS that were unexpectedly diagnosed: In addition to mutations in the X-chromosomal COL4A5 type IV collagen gene, nephrin and podocin polymorphisms aggravated kidney damage, leading to FSGS with ruptures of the basement membrane in a toddler and early renal failure in heterozygous girls. |
| 2081 | 30755075 | Abbreviations: ALB: albumin; ARHGDIB: Rho GDP dissociation inhibitor beta; APOL1: apolipoprotein L1; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG16L2: autophagy related 16 like 2; BECN1: beclin 1; CDKN1B: cyclin dependent kinase inhibitor 1B; CLEC16A, C-type lectin domain containing 16A; CYBB: cytochrome b-245 beta chain; DC: dendritic cell; DRAM1: DNA damage regulated autophagy modulator 1; eQTL: expression quantitative trait loci; GWAS: genome-wide association study; IFNA: interferon alpha; IRGM: immunity related GTPase M; LRRK2: leucine rich repeat kinase 2; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MTMR3: myotubularin related protein 3; LAP" LC3-associated phagocytosis; LN: lupus nephritis; NOD: non-obese diabetic; NPHS2: NPHS2, podocin; PBMC: peripheral blood mononuclear cell; RUBCN: rubicon autophagy regulator; SLE: systemic lupus erythematosus. |
| 2082 | 30841422 | The circulating levels of GLP-1/SDF-1α and protein levels of angiogenesis (VEGF/SDF-1α/CXCR4) and GLP-1R in kidney were progressively increased from groups 1 to 5, whereas circulating DPP4 activity exhibited an opposite pattern of SDF-1α among the groups (all p < 0.0001). |
| 2083 | 30841422 | The protein expressions of oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptosis (Bax/caspase-3/PARP), fibrosis (Smad3/TGF-ß) and inflammation (TNF-α/NF-κB/MMP-2) and kidney injury score displayed an opposite pattern, whereas the protein expressions of TMP2, endothelial-cell markers (CD31/eNOS) and podocyte integrity biomarkers (podocin/ZO-1/synaptopodin) exhibited an identical pattern of RBF among the groups (all p < 0.001). |
| 2084 | 30993911 | The results showed that salidroside treatment ameliorates proteinuria; improves expressions of nephrin and podocin; and reduces kidney fibrosis and glomerulosclerosis induced by ADR. |
| 2085 | 31060008 | SQ also significantly reduced the C3 and IgG depositions, and restored podocin and synaptopodin expressions. |
| 2086 | 31115515 | Enhanced TUG1 expression by exogenous recombinant vector regulated the expression of podocyte associated proteins [Nephrin, Podocin and CCAAT/enhancer‑binding protein (CHOP)]. |
| 2087 | 31115515 | The decreased Nephrin and Podocin expression, upregulated CHOP expression and the increased albumin influx were slightly enhanced by miR‑197 mimic transfection, while markedly suppressed by miR‑197 inhibitor transfection in LPS‑induced podocytes. |
| 2088 | 31115515 | However, the p38 MAPK inhibitor SB203580 reversed the changes that TUG1 induced in the levels of Beclin1, LC3 II/LC3 I and p62. |
| 2089 | 31115515 | Enhanced TUG1 expression by exogenous recombinant vector regulated the expression of podocyte associated proteins [Nephrin, Podocin and CCAAT/enhancer‑binding protein (CHOP)]. |
| 2090 | 31115515 | The decreased Nephrin and Podocin expression, upregulated CHOP expression and the increased albumin influx were slightly enhanced by miR‑197 mimic transfection, while markedly suppressed by miR‑197 inhibitor transfection in LPS‑induced podocytes. |
| 2091 | 31115515 | However, the p38 MAPK inhibitor SB203580 reversed the changes that TUG1 induced in the levels of Beclin1, LC3 II/LC3 I and p62. |
| 2092 | 31174067 | Circulatory inflammatory markers (TNF-α/MPO/IL-6/Ly6G/CD11b/c), histopathologic cerebro and renal changes and oxidative stress were determined. |
| 2093 | 31174067 | CRS group also demonstrated declined renal function, accelerated renal collagen deposition, fibrosis and compromised glomerular podocyte components (podocin/ZO-1/fibronectin/synaptopodin). |
| 2094 | 31191670 | Furthermore, these cells express the typical MSC markers CD73, CD90, and CD105. |
| 2095 | 31191670 | Immunofluorescence-based stainings of sectioned 3D-NPCs revealed cells expressing the renal progenitor cell markers (SIX2 and PAX8), podocyte markers (Nephrin and Podocin), the endothelial marker (CD31), and mesenchymal markers (Vimentin and PDGFR-β). |
| 2096 | 31200942 | These cells co-expressed the podocyte markers podocin, nephrin, p57 and VEGF164, but not markers of endothelial (ERG) or mesangial (Perlecan) cells. |
| 2097 | 31275420 | Anemoside B4 Protects Rat Kidney from Adenine-Induced Injury by Attenuating Inflammation and Fibrosis and Enhancing Podocin and Nephrin Expression. |
| 2098 | 31275420 | Moreover, IL-1β, IL-6, TNFα, and NFκB expression was upregulated in the kidney. |
| 2099 | 31275420 | Simultaneously, the expression of NLRP3 (the nucleotide-binding and oligomerization domain-like receptor, leucine-rich repeat and pyrin domain-containing 3) in the inflammasome, which consists of Caspase 1, ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), and IL-18, was significantly upregulated. |
| 2100 | 31275420 | B4 could significantly decrease BUN and Crea; reduce urinary proteins in rats; suppress the expression of IL-6, IL-1β, NFκB, NLRP3, Caspase 1, ASC, and IL-18; and increase urinary adenine contents and promote its excretion. |
| 2101 | 31275420 | In addition, B4 also upregulated the expression of podocin and nephrin, two major podocyte proteins, and reduced the fiber collagen in the renal interstitial, suggesting that B4 could protect the glomerular matrix from adenine injury in addition to its anti-inflammatory effects. |
| 2102 | 31275420 | Anemoside B4 Protects Rat Kidney from Adenine-Induced Injury by Attenuating Inflammation and Fibrosis and Enhancing Podocin and Nephrin Expression. |
| 2103 | 31275420 | Moreover, IL-1β, IL-6, TNFα, and NFκB expression was upregulated in the kidney. |
| 2104 | 31275420 | Simultaneously, the expression of NLRP3 (the nucleotide-binding and oligomerization domain-like receptor, leucine-rich repeat and pyrin domain-containing 3) in the inflammasome, which consists of Caspase 1, ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), and IL-18, was significantly upregulated. |
| 2105 | 31275420 | B4 could significantly decrease BUN and Crea; reduce urinary proteins in rats; suppress the expression of IL-6, IL-1β, NFκB, NLRP3, Caspase 1, ASC, and IL-18; and increase urinary adenine contents and promote its excretion. |
| 2106 | 31275420 | In addition, B4 also upregulated the expression of podocin and nephrin, two major podocyte proteins, and reduced the fiber collagen in the renal interstitial, suggesting that B4 could protect the glomerular matrix from adenine injury in addition to its anti-inflammatory effects. |
| 2107 | 31371698 | Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1. |
| 2108 | 31371698 | Herein, we aimed to study the roles of long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) and histone 3 lysine 27 trimethylation (H3K27me3) in DN. |
| 2109 | 31371698 | The roles of PVT1 and enhancer of zeste homolog 2 (EZH2) were validated via loss-of-function and gain-of-function in vitro experiments to identify the interactions among PVT1, EZH2, and forkhead box A1 (FOXA1). |
| 2110 | 31371698 | The podocyte damage and apoptosis due to PVT1 and FOXA1 were verified with in vivo experiments. |
| 2111 | 31371698 | A large number of CpG (C-phosphate-G) island sites were predicted at the FOXA1 promoter region, where PVT1 recruited EZH2 to promote the recruitment of H3K27me3. |
| 2112 | 31371698 | The silencing of PVT1 or the overexpression of FOXA1 relieved the damage and inhibited the apoptosis of podocytes in DN, as was evidenced by the upregulated expression of synaptopodin and podocin, higher expression of Bcl-2, and lower expression of Bax and cleaved caspase-3. |
| 2113 | 31371698 | The key findings of this study collectively indicate that the suppression of lncRNA PVT1 exerts inhibitory effects on podocyte damage and apoptosis via FOXA1 in DN, which is of clinical significance. |
| 2114 | 31394178 | Effect of shenyan xiaobai granule on nephrin and podocin of adriamycin-induced renal injury: A randomised controlled trial. |
| 2115 | 31441181 | The models of podocyte injury were verified to be successful as seen through significantly decreased levels of nephrin, podocin, and CD2AP and increased level of desmin. |
| 2116 | 31441181 | The sC5b-9-induced podocyte apoptosis was inhibited in injured podocytes treated with PrA and OA, accompanied by increased protein levels of nephrin, podocin, CD2AP, and Bcl2 and decreased levels of desmin and Bax. |
| 2117 | 31441181 | The p-AKT/p-mTOR levels were also reduced by treatment of PrA and OA while AKT/mTOR was unaltered. |
| 2118 | 31441181 | The models of podocyte injury were verified to be successful as seen through significantly decreased levels of nephrin, podocin, and CD2AP and increased level of desmin. |
| 2119 | 31441181 | The sC5b-9-induced podocyte apoptosis was inhibited in injured podocytes treated with PrA and OA, accompanied by increased protein levels of nephrin, podocin, CD2AP, and Bcl2 and decreased levels of desmin and Bax. |
| 2120 | 31441181 | The p-AKT/p-mTOR levels were also reduced by treatment of PrA and OA while AKT/mTOR was unaltered. |
| 2121 | 31502757 | By 72 hr after IR procedure, the circulatory levels of creatinine, blood urine nitrogen and inflammatory biomarkers (interleukin [IL]-6/tumor necrosis factor [TNF]-α), and ratio of urine protein to urine creatinine were significantly higher in Group 3 than in other groups and significantly higher in Group 4 than in Groups 1 and 2, but they showed no different between Groups 1 and 2 (all p < .001). |
| 2122 | 31502757 | The microscopic findings showed that the expressions of kidney injury score, cellular inflammation (MMP-9/CD14//F4/80), and fibrotic area were identical to the circulatory inflammation, whereas the integrity of podocyte components (ZO-1/synaptopodin/podocin) exhibited an opposite to circulatory inflammation among the four groups (all p < .0001). |
| 2123 | 31502757 | The protein expressions of inflammatory (TNF-α/IL-1ß/NF-κB/iNOS/TRAF6/MyD88/TLR-4), apoptotic/cell death (mitochondrial Bax/cleaved caspase-3/p-53), oxidized protein, mitogen-activated protein kinase family (p-38/p-JNK/p-c-JUN), and mitochondrial-damaged biomarkers displayed a similar pattern, whereas the antiapoptotic (Bcl-2/Bcl-XL) and integrity of mitochondrial biomarkers followed an opposite trend to circulatory inflammation among the four groups (all p < .001). |
| 2124 | 31529341 | TRPC6 and NPHS2 gene variants in adult patients with steroid-resistant nephrotic syndrome in North-West of Iran. |
| 2125 | 31529341 | Whole exons of NPHS2 gene and -254 C > G, -218 C > T, and -361 A > T polymorphisms in the promoter of TRPC6 gene were studied. |
| 2126 | 31529341 | Podocin related mutations are not too much associated with SRNS in adults, but we should consider the possibility of TRPC6 gene mutation in this population. |
| 2127 | 31529341 | TRPC6 and NPHS2 gene variants in adult patients with steroid-resistant nephrotic syndrome in North-West of Iran. |
| 2128 | 31529341 | Whole exons of NPHS2 gene and -254 C > G, -218 C > T, and -361 A > T polymorphisms in the promoter of TRPC6 gene were studied. |
| 2129 | 31529341 | Podocin related mutations are not too much associated with SRNS in adults, but we should consider the possibility of TRPC6 gene mutation in this population. |
| 2130 | 31529341 | TRPC6 and NPHS2 gene variants in adult patients with steroid-resistant nephrotic syndrome in North-West of Iran. |
| 2131 | 31529341 | Whole exons of NPHS2 gene and -254 C > G, -218 C > T, and -361 A > T polymorphisms in the promoter of TRPC6 gene were studied. |
| 2132 | 31529341 | Podocin related mutations are not too much associated with SRNS in adults, but we should consider the possibility of TRPC6 gene mutation in this population. |
| 2133 | 31532378 | The main actor of the glomerular filter is the podocyte whose interlaced pedicels bear protein complexes (nephrin, podocin, etc.) creating a molecular sieve (slit diaphragm) to achieve the filtration. |
| 2134 | 31535208 | Saxagliptin attenuates glomerular podocyte injury by increasing the expression of renal nephrin and podocin in type 2 diabetic rats. |
| 2135 | 31566426 | Urinary nephrin shedding indicated loss of the glomerular slit diaphragm, which also correlates with the dramatic elevation in albuminuria and loss of podocin staining in aged T2DN rats. |
| 2136 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2137 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2138 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2139 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2140 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2141 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2142 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2143 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2144 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2145 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2146 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2147 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2148 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2149 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2150 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2151 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2152 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2153 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2154 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2155 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2156 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2157 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2158 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2159 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2160 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2161 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2162 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2163 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2164 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2165 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2166 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2167 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2168 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2169 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2170 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2171 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2172 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2173 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2174 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2175 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2176 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2177 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2178 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2179 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2180 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2181 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2182 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2183 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2184 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2185 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2186 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2187 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2188 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2189 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2190 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2191 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2192 | 31566428 | High glucose reduces expression of podocin in cultured human podocytes by stimulating TRPC6. |
| 2193 | 31566428 | The transient receptor potential canonical 6 (TRPC6) channel and podocin are colocalized in the glomerular slit diaphragm as an important complex to maintain podocyte function. |
| 2194 | 31566428 | Gain of TRPC6 function and loss of podocin function induce podocyte injury. |
| 2195 | 31566428 | We have previously shown that high glucose induces apoptosis of podocytes by activating TRPC6; however, whether the activated TRPC6 can alter podocin expression remains unknown. |
| 2196 | 31566428 | Western blot analysis and confocal microscopy were used to examine both expression levels of TRPC6, podocin, and nephrin and morphological changes of podocytes in response to high glucose. |
| 2197 | 31566428 | High glucose increased the expression of TRPC6 but reduced the expression of podocin and nephrin, in both cultured human podocytes and type 1 diabetic rat kidneys. |
| 2198 | 31566428 | The decreased podocin was diminished in TRPC6 knockdown podocytes. |
| 2199 | 31566428 | These data together suggest that high glucose reduces protein levels of podocin by activating TRPC6 and induces morphological changes of cultured podocytes. |
| 2200 | 31637677 | In addition, the results showed downregulation effect of AuNPs in renal mRNA or protein expression of transforming growth factor β1 (TGF-β1), fibronectin, collagen IV, tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor-A (VEGF-A). |
| 2201 | 31637677 | Moreover, the protein expression of nephrin and podocin, podocyte markers, in glomeruli was increased in the AuNPs + D group compared with the D group. |
| 2202 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2203 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2204 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2205 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2206 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2207 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2208 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2209 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2210 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2211 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2212 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2213 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2214 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2215 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2216 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2217 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2218 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2219 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2220 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2221 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2222 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2223 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2224 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2225 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2226 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2227 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2228 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2229 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2230 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2231 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2232 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2233 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2234 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2235 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2236 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2237 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2238 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2239 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2240 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2241 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2242 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2243 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2244 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2245 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2246 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2247 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2248 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2249 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2250 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2251 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2252 | 31638199 | Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury. |
| 2253 | 31638199 | Numerous studies have reported that angiotensin (Ang) II, nephrin, and podocin serve pivotal roles in podocyte injury, and thus can lead to the occurrence of proteinuria and the progression of kidney diseases. |
| 2254 | 31638199 | This study aimed to investigate the effects of Ang II on the production of nephrin and podocin, and their relationship with podocyte injury. |
| 2255 | 31638199 | We also aimed to determine whether nephrin, podocin and caspase‑9 production depends on the PI3K/Akt/nuclear factor (NF)‑κB signaling pathway in cultured mouse podocytes. |
| 2256 | 31638199 | Cells were treated with 10‑6 mol/l of Ang II and/or LY294002 (inhibitor of Akt) or 740Y‑P (activator of PI3K) for 48 h to detect Akt, phosphorylated (phospho)‑Akt, p65 NF‑κB, and phospho‑p65 NF‑κB, nephrin, podocin and caspase‑9 expression, and podocyte apoptosis. |
| 2257 | 31638199 | Ang II decreased phospho‑Akt, phospho‑p65 NF‑κB, nephrin, and podocin and increased caspase‑9 expression, while podocyte apoptosis was promoted. |
| 2258 | 31638199 | LY294002 further enhanced Ang II‑induced downregulation of Akt and p65 NF‑κB activation, as well as upregulation of caspase‑9 mRNA and protein, and promoted the apoptosis of podocytes. |
| 2259 | 31638199 | Of note, 740Y‑P restored Ang II‑induced downregulation of Akt and p65 NF‑κB activation, and upregulation of caspase‑9, and decreased podocyte apoptosis. |
| 2260 | 31638199 | The data suggested that Ang II could regulate the expression of nephrin, podocin and caspase‑9. |
| 2261 | 31638199 | Collectively, our findings suggested that the PI3K/Akt/NF‑κB survival axis may serve a pivotal role in podocyte injury. |
| 2262 | 31853790 | The mechanisms underlying the increase of albumin permeability are probably due to endothelial cell damage as an initial event, which was demonstrated by the decrease of Platelet endothelial cell adhesion molecule (PECAM-1 or CD31), while the podocytes' expressions of synaptopodin and podocin were normal. |
| 2263 | 31862892 | In addition, mSC treatment recovered WT1 expression, improved nephrin, podocin, synaptopodin, podocalyxin, and VEGF expression, and downregulated proinflammatory Th1 cytokines in the kidney with a shift towards regulatory Th2 cytokines. |
| 2264 | 31865844 | Instead we present data showing that autophagy in podocytes is mainly controlled by AMP-activated protein kinase (AMPK) and ULK1 (unc-51 like kinase 1). |
| 2265 | 31865844 | Abbreviations: AICAR: 5-aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy related; BW: body weight; Cq: chloroquine; ER: endoplasmic reticulum; ESRD: end stage renal disease; FACS: fluorescence activated cell sorting; GFP: green fluorescent protein; i.p.: intra peritoneal; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; NPHS1: nephrosis 1, nephrin; NPHS2: nephrosis 2, podocin; PLA: proximity-ligation assay; PRKAA: 5'-AMP-activated protein kinase catalytic subunit alpha; RPTOR/RAPTOR: regulatory associated protein of MTOR, complex 1; RFP: red fluorescent protein; TSC1: tuberous sclerosis 1; ULK1: unc-51 like kinase 1. |
| 2266 | 31881024 | Using double immunofluorescence (IF) followed by digital image analysis, kidney sections were stained for fibrin(ogen) and CD41 (marker for platelets), von-Willebrand factor (marker for endothelial cells and platelets), and podocin (marker for podocytes). |
| 2267 | 31954110 | It showed that D1R and podocyte-associated proteins (Podocin, CD2AP and Nephrin) expression were significantly decreased both in the T1D mice (fed for 8 and 12 weeks) and HG-cultured MPC5 cells, while the NOX-5 expression increased. |
| 2268 | 31966749 | Western blots were carried out for the related protein expression in podocytes, including CXCR3, Nephrin, Podocin, Bcl-2, Bax, and Caspase-3. |
| 2269 | 31966749 | Moreover, knockdown of CXCR3 reduced the podocytes injury in cell apoptosis and inflammation through increasing the expression of Nephrin, Podocin and Bcl-2, and decreasing the expression of Bax and Caspase-3. |
| 2270 | 31966749 | Western blots were carried out for the related protein expression in podocytes, including CXCR3, Nephrin, Podocin, Bcl-2, Bax, and Caspase-3. |
| 2271 | 31966749 | Moreover, knockdown of CXCR3 reduced the podocytes injury in cell apoptosis and inflammation through increasing the expression of Nephrin, Podocin and Bcl-2, and decreasing the expression of Bax and Caspase-3. |
| 2272 | 32020343 | Nephrin, NEPH1, P-cadherin, FAT, and ephrin-B1 were reported to be extracellular components forming a molecular sieve of the slit diaphragm. |
| 2273 | 32020343 | Several cytoplasmic proteins such as ZO-1, podocin, CD2AP, MAGI proteins and Par-complex molecules were identified as scaffold proteins linking the slit diaphragm to the cytoskeleton. |
| 2274 | 32020343 | The recent studies on the signaling pathway from nephrin, NEPH1, and ephrin-B1 were reviewed. |
| 2275 | 32028827 | Western blot analysis indicated that it could restore the expression of RhoA, ROCK and vimentin, nephrin, podocin and p65 and IκBα phosphorylation. |
| 2276 | 32029775 | Western blot analysis showed that GSJD could regulate the mitochondrial apoptotic pathway by downregulating the expression of Bax and upregulating the expression of BCL-2 in the kidneys of DN rats. |
| 2277 | 32029775 | Moreover, the Akt pathway, an upstream signalling pathway of the BCL-2 family, was also ameliorated by GSJD. |
| 2278 | 32029775 | Further, the podocyte foot process markers podocin and nephrin were upregulated by GSJD in DN rats. |
| 2279 | 32048472 | Differentiation of nephrin (NPHS1)-green fluorescent protein (GFP) iPSCs into kidney podocytes (iPSC-PODs) was performed by the addition of Activin A, bone morphogenetic protein 7 (BMP7), and retinoic acid over 10 days of culture. |
| 2280 | 32048472 | The transplanted cells were viable and located in the outer nephrogenic zone where they were found to colocalize with, or sit adjacent to, cells positive for glomerular-specific markers including podocin, synaptopodin, and Wilms' tumor 1 (WT1). |
| 2281 | 32090080 | In the model group, the Psoriasis Area and Severity Index (PASI) scores of scaly and erythema obviously increased (p < 0.01), creatinine and blood urea nitrogen significantly increased (p < 0.01), the positive area of hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining in kidney increased (p < 0.01), malondialdehyde significantly increased with superoxide dismutase (SOD) decreased (p < 0.01), 24-hour urine protein increased and the expressions of podocin and CD2 associate protein (CD2AP) decreased (p < 0.01), and kidney/serum inflammatory factors (IL-17, IL-1β, IL-6, TNF-α, and IL-22) and TLR/NF-κB-related expression (TLR2, TLR4, MyD88, and NF-κBp65) all increased (p < 0.01). |
| 2282 | 32129207 | When we correlated the NPHS2 mutation status with disease progression, there was a statistically significant increase in serum creatinine, proteinuria, and serum albumin values in patients with NPHS2 gene mutations compared to the group without mutation (P <0.05). |
| 2283 | 32167144 | In vivo, wild-type (WT) mice developed heavy proteinuria and kidney dysfunction following Adriamycin insult, concomitant with focal segmental glomerulosclerosis (FSGS) and podocytopathy, marked by loss of podocin and synaptopodin, podocytopenia and extensive foot process effacement on electron microscopy. |
| 2284 | 32249272 | RT-PCR was performed for assessing nephrin, podocin, IL-6, CD68, Collagen-1, and TGF-β1 mRNA expressions. |
| 2285 | 32249272 | SND2 group showed not only significantly lower CD68, IL-6, Collagen-1, and TGF-β1 mRNA expressions, but also higher mRNA expressions of nephrin and podocin. |
| 2286 | 32285909 | TPL inhibited FSGS-induced cell apoptosis in rats and regulated IL4, nephrin, podocin, and p53 protein levels via using CCK8, TUNEL, and Western blot assays. |
| 2287 | 32285909 | TPL treatment increased the expression of nephrin and podocin and decreased p53 expression in rat podocytes. |
| 2288 | 32285909 | TPL inhibited FSGS-induced cell apoptosis in rats and regulated IL4, nephrin, podocin, and p53 protein levels via using CCK8, TUNEL, and Western blot assays. |
| 2289 | 32285909 | TPL treatment increased the expression of nephrin and podocin and decreased p53 expression in rat podocytes. |
| 2290 | 32307498 | Activities of SOD, CAT and GPx and the content of MDA in renal tissues were assayed. |
| 2291 | 32307498 | Pathological changes in renal tissues were observed by HE staining, PAS staining, PASM staining, Masson staining and transmission electron microscopy. p-NF-κB p65, TNF-α, TGF-β1, collagen IV, nephrin and podocin protein expressed in renal tissues were determined by immunohistochemistry and western blotting. |
| 2292 | 32307498 | Results showed that FA significantly improved the kidney organ coefficient, decreased the UP, BUN, Cr, FBG, TC and TG levels in serum, increased SOD, CAT and GPx activities, reduced MDA content in renal tissues and alleviated pathological injury of the renal tissues. |
| 2293 | 32307498 | What's more, long-term treatment with FA considerably down-regulated the expressions of p-NF-κB p65, TNF-α, TGF-β1 and collagen IV proteins, and up-regulated the expressions of nephrin and podocin proteins in renal tissues. |
| 2294 | 32307498 | Activities of SOD, CAT and GPx and the content of MDA in renal tissues were assayed. |
| 2295 | 32307498 | Pathological changes in renal tissues were observed by HE staining, PAS staining, PASM staining, Masson staining and transmission electron microscopy. p-NF-κB p65, TNF-α, TGF-β1, collagen IV, nephrin and podocin protein expressed in renal tissues were determined by immunohistochemistry and western blotting. |
| 2296 | 32307498 | Results showed that FA significantly improved the kidney organ coefficient, decreased the UP, BUN, Cr, FBG, TC and TG levels in serum, increased SOD, CAT and GPx activities, reduced MDA content in renal tissues and alleviated pathological injury of the renal tissues. |
| 2297 | 32307498 | What's more, long-term treatment with FA considerably down-regulated the expressions of p-NF-κB p65, TNF-α, TGF-β1 and collagen IV proteins, and up-regulated the expressions of nephrin and podocin proteins in renal tissues. |
| 2298 | 32478392 | At day 6, diseased animals treated with KH-3 showed significant reduction in glomerular HuR levels, proteinuria, podocyte injury determined by ameliorated podocyte loss and podocin expression, glomerular staining for periodic acid-Schiff positive extracellular matrix proteins, fibronectin and collagen IV and mRNA and protein levels of profibrotic markers, compared with untreated disease rats. |
| 2299 | 32617419 | Several proteins including podocin, nephrin, CD2AP, and TRPC6 form a macromolecular assembly and constitute the slit-diaphragm. |
| 2300 | 32617419 | Podocin shares 44% homology with stomatin family proteins and similar to the stomatin proteins, podocin was shown to associate into higher-order oligomers at the site of slit-diaphragm. |
| 2301 | 32617419 | Several proteins including podocin, nephrin, CD2AP, and TRPC6 form a macromolecular assembly and constitute the slit-diaphragm. |
| 2302 | 32617419 | Podocin shares 44% homology with stomatin family proteins and similar to the stomatin proteins, podocin was shown to associate into higher-order oligomers at the site of slit-diaphragm. |
| 2303 | 32686524 | A number of key proteins are essential for podocyte function, including nephrin, podocin, CD2-associated protein (CD2AP), synaptopodin, and α-actinin-4 (ACTN4). |
| 2304 | 32716365 | The hiPS cell-derived podocytes produced by this method express lineage-specific markers (including nephrin, podocin, and Wilm's Tumor 1) and exhibit the specialized morphological characteristics (including primary and secondary foot processes) associated with mature and functional podocytes. |
| 2305 | 32739208 | Urine pellet podocin and aquaporin2 mRNAs normalized to the urine creatinine concentration (UPod:Creat ratio and UAqp2:Creat ratio) were used as markers of podocyte detachment and tubular injury, respectively. |
| 2306 | 32739208 | The ratio of two podocyte mRNA markers, podocin to nephrin (UPod:Neph) as well as the ratio of podocin to the tubular marker aquaporin2 (UPod:Aqp2) estimated the relative rates of podocyte stress and glomerular vs. tubular injury. |
| 2307 | 32739208 | Urine pellet podocin and aquaporin2 mRNAs normalized to the urine creatinine concentration (UPod:Creat ratio and UAqp2:Creat ratio) were used as markers of podocyte detachment and tubular injury, respectively. |
| 2308 | 32739208 | The ratio of two podocyte mRNA markers, podocin to nephrin (UPod:Neph) as well as the ratio of podocin to the tubular marker aquaporin2 (UPod:Aqp2) estimated the relative rates of podocyte stress and glomerular vs. tubular injury. |
| 2309 | 32765784 | Lycopene attenuates high glucose-mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway. |
| 2310 | 32765784 | To explore the effects of Lyc on the PI3K/AKT signaling pathway and autophagy, LY294002 (LY) and 3-methyladenine (3-MA) were used as PI3K and autophagy inhibitors, respectively. |
| 2311 | 32765784 | The expression levels of nephrin, podocin, apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase-3), autophagy-related proteins [Beclin-1 and microtubule associated protein 1 light chain 3 (LC3)II/LC3I] and certain key proteins involved in the PI3K/AKT signaling pathway were measured via western blotting. |
| 2312 | 32765784 | The results suggested that Lyc reversed the inhibitory effect of HG on cell viability, and the protein expression levels of nephrin and podocin, as well as the promoting effect of HG on MPC5 podocyte apoptosis. |
| 2313 | 32765784 | In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG- and LY-mediated MPC5 podocyte apoptosis. |
| 2314 | 32765784 | Therefore, the present study suggested that Lyc may protect against HG-induced MPC5 podocyte apoptosis by promoting autophagy activity via activation of the PI3K/AKT signaling pathway. |
| 2315 | 32765784 | Lycopene attenuates high glucose-mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway. |
| 2316 | 32765784 | To explore the effects of Lyc on the PI3K/AKT signaling pathway and autophagy, LY294002 (LY) and 3-methyladenine (3-MA) were used as PI3K and autophagy inhibitors, respectively. |
| 2317 | 32765784 | The expression levels of nephrin, podocin, apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase-3), autophagy-related proteins [Beclin-1 and microtubule associated protein 1 light chain 3 (LC3)II/LC3I] and certain key proteins involved in the PI3K/AKT signaling pathway were measured via western blotting. |
| 2318 | 32765784 | The results suggested that Lyc reversed the inhibitory effect of HG on cell viability, and the protein expression levels of nephrin and podocin, as well as the promoting effect of HG on MPC5 podocyte apoptosis. |
| 2319 | 32765784 | In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG- and LY-mediated MPC5 podocyte apoptosis. |
| 2320 | 32765784 | Therefore, the present study suggested that Lyc may protect against HG-induced MPC5 podocyte apoptosis by promoting autophagy activity via activation of the PI3K/AKT signaling pathway. |
| 2321 | 32786113 | The serum from patients with DN significantly increased FOXO3a and its downstream genes FasL and Bim, thereby inducing the high level of cleaved caspase3 and the loss of nephrin and podocin expressions in podocytes. |
| 2322 | 32786113 | Downregulation of FOXO3a decreased AOPPs-induced podocyte apoptosis and restored the levels of podocyte markers nephrin and podocin, and upregulation of FOXO3a exacerbated these changes in podocytes after AOPPs treatment. |
| 2323 | 32786113 | Moreover AOPPs activated the accumulated FOXO3a by maintaining FOXO3a in the nucleus, and this process was dependent on ROS-mediated AKT signaling deactivation. |
| 2324 | 32786113 | The serum from patients with DN significantly increased FOXO3a and its downstream genes FasL and Bim, thereby inducing the high level of cleaved caspase3 and the loss of nephrin and podocin expressions in podocytes. |
| 2325 | 32786113 | Downregulation of FOXO3a decreased AOPPs-induced podocyte apoptosis and restored the levels of podocyte markers nephrin and podocin, and upregulation of FOXO3a exacerbated these changes in podocytes after AOPPs treatment. |
| 2326 | 32786113 | Moreover AOPPs activated the accumulated FOXO3a by maintaining FOXO3a in the nucleus, and this process was dependent on ROS-mediated AKT signaling deactivation. |
| 2327 | 32800553 | Expression of podocyte proteins Wilms tumor 1 (WT1) and podocin were decreased, while expression of collagen 1 (COL1) and transforming growth factor-beta1 (TGF-β1) were increased on Western blotting. |
| 2328 | 32840752 | Downregulation of megalin, cubilin, ClC-5 and podocin in Fabry nephropathy: potential implications in the decreased effectiveness of enzyme replacement therapy. |
| 2329 | 32840752 | We report in a male and a female patient the decreased expression of megalin, cubilin, ClC-5 and podocin compared to controls and chronic kidney disease (CKD) biopsies. |
| 2330 | 32840752 | Downregulation of megalin, cubilin, ClC-5 and podocin in Fabry nephropathy: potential implications in the decreased effectiveness of enzyme replacement therapy. |
| 2331 | 32840752 | We report in a male and a female patient the decreased expression of megalin, cubilin, ClC-5 and podocin compared to controls and chronic kidney disease (CKD) biopsies. |
| 2332 | 32858527 | PECs differentiated to a podocyte fate had ultrastructural features of podocytes and co-expressed the podocyte markers podocin, nephrin, p57 and VEGF164, but not markers of mesangial (Perlecan) or endothelial (ERG) cells. |
| 2333 | 32896839 | Overexpression of Linc 4930556M19Rik Suppresses High Glucose-Triggered Podocyte Apoptosis, Fibrosis and Inflammation via the miR-27a-3p/Metalloproteinase 3 (TIMP3) Axis in Diabetic Nephropathy. |
| 2334 | 32896839 | Western blot assay was used to assessed levels of fibrosis-related proteins, podocin, and tissue inhibitor of metalloproteinase 3 (TIMP3). |
| 2335 | 32896839 | Moreover, TIMP3 was the target for miR-27a-3p and miR-27a-3p inhibition slowed podocyte injury by targeting TIMP3. |
| 2336 | 32907879 | Proteolytic cleavage of Podocin by Matriptase exacerbates podocyte injury. |
| 2337 | 32907879 | The mechanism could be accounted for by an imbalance favoring Matriptase over its cognate inhibitor, hepatocyte growth factor activator inhibitor type 1 (HAI-1), because conditional depletion of HAI-1 in podocytes accelerated podocyte injury in mouse model. |
| 2338 | 32907879 | Matriptase was capable of cleaving Podocin, but such a reaction was blocked by either HAI-1 or dominant-negative Matriptase. |
| 2339 | 32907879 | Furthermore, the N terminus of Podocin, as a consequence of Matriptase cleavage of Podocin, translocated to nucleoli, suggesting that the N terminus of Podocin might be involved in the process of podocyte injury. |
| 2340 | 32907879 | Given these observations, we propose that the proteolytic cleavage of Podocin by Matriptase could potentially cause podocyte injury and that targeting Matriptase could be a novel therapeutic strategy for CKD patients. |
| 2341 | 32907879 | Proteolytic cleavage of Podocin by Matriptase exacerbates podocyte injury. |
| 2342 | 32907879 | The mechanism could be accounted for by an imbalance favoring Matriptase over its cognate inhibitor, hepatocyte growth factor activator inhibitor type 1 (HAI-1), because conditional depletion of HAI-1 in podocytes accelerated podocyte injury in mouse model. |
| 2343 | 32907879 | Matriptase was capable of cleaving Podocin, but such a reaction was blocked by either HAI-1 or dominant-negative Matriptase. |
| 2344 | 32907879 | Furthermore, the N terminus of Podocin, as a consequence of Matriptase cleavage of Podocin, translocated to nucleoli, suggesting that the N terminus of Podocin might be involved in the process of podocyte injury. |
| 2345 | 32907879 | Given these observations, we propose that the proteolytic cleavage of Podocin by Matriptase could potentially cause podocyte injury and that targeting Matriptase could be a novel therapeutic strategy for CKD patients. |
| 2346 | 32907879 | Proteolytic cleavage of Podocin by Matriptase exacerbates podocyte injury. |
| 2347 | 32907879 | The mechanism could be accounted for by an imbalance favoring Matriptase over its cognate inhibitor, hepatocyte growth factor activator inhibitor type 1 (HAI-1), because conditional depletion of HAI-1 in podocytes accelerated podocyte injury in mouse model. |
| 2348 | 32907879 | Matriptase was capable of cleaving Podocin, but such a reaction was blocked by either HAI-1 or dominant-negative Matriptase. |
| 2349 | 32907879 | Furthermore, the N terminus of Podocin, as a consequence of Matriptase cleavage of Podocin, translocated to nucleoli, suggesting that the N terminus of Podocin might be involved in the process of podocyte injury. |
| 2350 | 32907879 | Given these observations, we propose that the proteolytic cleavage of Podocin by Matriptase could potentially cause podocyte injury and that targeting Matriptase could be a novel therapeutic strategy for CKD patients. |
| 2351 | 32907879 | Proteolytic cleavage of Podocin by Matriptase exacerbates podocyte injury. |
| 2352 | 32907879 | The mechanism could be accounted for by an imbalance favoring Matriptase over its cognate inhibitor, hepatocyte growth factor activator inhibitor type 1 (HAI-1), because conditional depletion of HAI-1 in podocytes accelerated podocyte injury in mouse model. |
| 2353 | 32907879 | Matriptase was capable of cleaving Podocin, but such a reaction was blocked by either HAI-1 or dominant-negative Matriptase. |
| 2354 | 32907879 | Furthermore, the N terminus of Podocin, as a consequence of Matriptase cleavage of Podocin, translocated to nucleoli, suggesting that the N terminus of Podocin might be involved in the process of podocyte injury. |
| 2355 | 32907879 | Given these observations, we propose that the proteolytic cleavage of Podocin by Matriptase could potentially cause podocyte injury and that targeting Matriptase could be a novel therapeutic strategy for CKD patients. |
| 2356 | 32908940 | The present study explored the effects of Tha on mRNA and protein expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 in HG-activated macrophages. iNOS and TNF-α are established as markers of classically activated macrophage (M1). |
| 2357 | 32908940 | CD206 and Arg-1 are regarded as markers of alternatively activated macrophages (M2). |
| 2358 | 32908940 | TNF-α and interleukin- (IL-) 1β levels as well as protein expressions of nephrin and podocin in HG, (HG) MS, and (Tha) MS-cultured podocytes were evaluated. |
| 2359 | 32908940 | The results showed that compared to the 11.1 mM normal glucose (NG), the 33.3 mM HG-cultured RAW 264.7 cells exhibited upregulated iNOS and TNF-α mRNAs and protein expressions, and downregulated CD206 and Arg-1 expressions significantly (p < 0.05). |
| 2360 | 32908940 | Tha 200 μg/ml suppressed iNOS and TNF-α, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05). |
| 2361 | 32908940 | Furthermore, (HG) MS-treated podocytes showed an increase in TNF-α and IL-1β levels and a downregulation in nephrin and podocin expression significantly compared to NG-treated and HG-treated podocytes (p < 0.05). |
| 2362 | 32908940 | The (Tha 200 μg/ml) MS group exhibited a decrease in TNF-α and IL-1β level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05). |
| 2363 | 32908940 | Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-α and IL-1β levels via its modulation on M1/M2 differentiation. |
| 2364 | 32908940 | The present study explored the effects of Tha on mRNA and protein expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 in HG-activated macrophages. iNOS and TNF-α are established as markers of classically activated macrophage (M1). |
| 2365 | 32908940 | CD206 and Arg-1 are regarded as markers of alternatively activated macrophages (M2). |
| 2366 | 32908940 | TNF-α and interleukin- (IL-) 1β levels as well as protein expressions of nephrin and podocin in HG, (HG) MS, and (Tha) MS-cultured podocytes were evaluated. |
| 2367 | 32908940 | The results showed that compared to the 11.1 mM normal glucose (NG), the 33.3 mM HG-cultured RAW 264.7 cells exhibited upregulated iNOS and TNF-α mRNAs and protein expressions, and downregulated CD206 and Arg-1 expressions significantly (p < 0.05). |
| 2368 | 32908940 | Tha 200 μg/ml suppressed iNOS and TNF-α, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05). |
| 2369 | 32908940 | Furthermore, (HG) MS-treated podocytes showed an increase in TNF-α and IL-1β levels and a downregulation in nephrin and podocin expression significantly compared to NG-treated and HG-treated podocytes (p < 0.05). |
| 2370 | 32908940 | The (Tha 200 μg/ml) MS group exhibited a decrease in TNF-α and IL-1β level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05). |
| 2371 | 32908940 | Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-α and IL-1β levels via its modulation on M1/M2 differentiation. |
| 2372 | 32908940 | The present study explored the effects of Tha on mRNA and protein expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 in HG-activated macrophages. iNOS and TNF-α are established as markers of classically activated macrophage (M1). |
| 2373 | 32908940 | CD206 and Arg-1 are regarded as markers of alternatively activated macrophages (M2). |
| 2374 | 32908940 | TNF-α and interleukin- (IL-) 1β levels as well as protein expressions of nephrin and podocin in HG, (HG) MS, and (Tha) MS-cultured podocytes were evaluated. |
| 2375 | 32908940 | The results showed that compared to the 11.1 mM normal glucose (NG), the 33.3 mM HG-cultured RAW 264.7 cells exhibited upregulated iNOS and TNF-α mRNAs and protein expressions, and downregulated CD206 and Arg-1 expressions significantly (p < 0.05). |
| 2376 | 32908940 | Tha 200 μg/ml suppressed iNOS and TNF-α, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p < 0.05). |
| 2377 | 32908940 | Furthermore, (HG) MS-treated podocytes showed an increase in TNF-α and IL-1β levels and a downregulation in nephrin and podocin expression significantly compared to NG-treated and HG-treated podocytes (p < 0.05). |
| 2378 | 32908940 | The (Tha 200 μg/ml) MS group exhibited a decrease in TNF-α and IL-1β level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p < 0.05). |
| 2379 | 32908940 | Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-α and IL-1β levels via its modulation on M1/M2 differentiation. |
| 2380 | 32968210 | We showed that the expression levels of caspase-11 and cleavage of gasdermin D (GSDMD-N) in podocytes were significantly elevated, accompanied by reduced expression of podocyte makers nephrin and podocin, loss and fusion in podocyte foot processes, increased inflammatory cytokines NF-κB, IL-1β, and IL-18, macrophage infiltration, glomerular matrix expansion and increased urinary albumin to creatinine ratio (UACR). |
| 2381 | 32968210 | Cultured human and mouse podocytes were treated with high glucose (30 mM), which significantly increased the expression levels of caspase-11 or caspase-4 (the homolog of caspase-11 in human), GSDMD-N, NF-κB, IL-1β, and IL-18, and decreased the expression of nephrin and podocin. |
| 2382 | 32968210 | We showed that the expression levels of caspase-11 and cleavage of gasdermin D (GSDMD-N) in podocytes were significantly elevated, accompanied by reduced expression of podocyte makers nephrin and podocin, loss and fusion in podocyte foot processes, increased inflammatory cytokines NF-κB, IL-1β, and IL-18, macrophage infiltration, glomerular matrix expansion and increased urinary albumin to creatinine ratio (UACR). |
| 2383 | 32968210 | Cultured human and mouse podocytes were treated with high glucose (30 mM), which significantly increased the expression levels of caspase-11 or caspase-4 (the homolog of caspase-11 in human), GSDMD-N, NF-κB, IL-1β, and IL-18, and decreased the expression of nephrin and podocin. |
| 2384 | 33011273 | NADPH oxidases (NOXs) are comprised of different isoforms, NOX1 to 5 and Duox1 and 2, and they trigger diabetic nephropathy (DN) in the patients with diabetes mellitus. |
| 2385 | 33011273 | Increased NOX5 mRNA expressions, increased desmin levels, and reduced podocin protein expressions in the kidney of NOX5 pod + mice were also significantly restored to normal levels by APX-115 treatment. |
| 2386 | 33024228 | Western blot and immunocytochemistry confirmed the alteration in the protein expression of tubulin, vimentin, podocin, cofilin-1, vinculin, E-cadherin, nephrin, VCAM-1, tenascin-C, and β-catenin. |
| 2387 | 33097787 | Podocyte stress (Urinary pellet podocin:nephrin mRNA ratio), podocyte detachment (Urinary pellet podocin mRNA:creatinine ratio: UPPod:CR) and a tubular marker (Urinary pellet aquaporin 2:creatinine ratio) were measured in macro-albuminuric, micro-albuminuric and norm-albuminuric groups. eGFR was reassessed after 4 years in 124 available diabetic subjects. |
| 2388 | 33155094 | Immunohistochemically stained with integrin α3β1, type IV collagen, laminin, nephrin, CD2-associated protein (CD2AP) and podocin to show the filtration barrier structure. |
| 2389 | 33155094 | Immunohistochemical results showed an increase in nephrin, podocin, CD2AP, laminin and a decrease in integrin α3β1 and type IV collagen. |
| 2390 | 33155094 | Immunohistochemically stained with integrin α3β1, type IV collagen, laminin, nephrin, CD2-associated protein (CD2AP) and podocin to show the filtration barrier structure. |
| 2391 | 33155094 | Immunohistochemical results showed an increase in nephrin, podocin, CD2AP, laminin and a decrease in integrin α3β1 and type IV collagen. |
| 2392 | 33202982 | Further, tangeretin enhanced the expression of the podocyte slit diaphragm proteins of nephrin and podocin down-regulated by glucose stimulation. |
| 2393 | 33235726 | The expression of regulator of calcineurin 1 and the podocin to nephrin ratio (PNR) were also increased in the PAN nephritis model. |
| 2394 | 33235726 | Furthermore, PNR in urinary NVs of Zucker diabetic fatty rats, a diabetic kidney disease model, was correlated with urinary albumin excretion (P<0.01). |
| 2395 | 33305316 | NPHS2 gene polymorphism aggravates renal damage caused by focal segmental glomerulosclerosis with COL4A3 mutation. |
| 2396 | 33305316 | Results revealed that nephrosis 2 (NPHS2) gene polymorphism aggravated renal damage in three FSGS families with heterozygous COL4A3 mutation, leading to early renal failure in index patients. |
| 2397 | 33305316 | Our findings suggest that COL4A3 and NPHS2 may have a synergistic effect on renal injury caused by FSGS. |
| 2398 | 33305316 | NPHS2 gene polymorphism aggravates renal damage caused by focal segmental glomerulosclerosis with COL4A3 mutation. |
| 2399 | 33305316 | Results revealed that nephrosis 2 (NPHS2) gene polymorphism aggravated renal damage in three FSGS families with heterozygous COL4A3 mutation, leading to early renal failure in index patients. |
| 2400 | 33305316 | Our findings suggest that COL4A3 and NPHS2 may have a synergistic effect on renal injury caused by FSGS. |
| 2401 | 33305316 | NPHS2 gene polymorphism aggravates renal damage caused by focal segmental glomerulosclerosis with COL4A3 mutation. |
| 2402 | 33305316 | Results revealed that nephrosis 2 (NPHS2) gene polymorphism aggravated renal damage in three FSGS families with heterozygous COL4A3 mutation, leading to early renal failure in index patients. |
| 2403 | 33305316 | Our findings suggest that COL4A3 and NPHS2 may have a synergistic effect on renal injury caused by FSGS. |
| 2404 | 33343355 | Bu-Shen-Huo-Xue Decoction Ameliorates Diabetic Nephropathy by Inhibiting Rac1/PAK1/p38MAPK Signaling Pathway in High-Fat Diet/Streptozotocin-Induced Diabetic Mice. |
| 2405 | 33343355 | Markers of podocyte epithelial-mesenchymal transition and the Rac1/PAK1/p38MAPK signaling pathway were evaluated to investigate the mechanism underlying function of BSHX decoction. |
| 2406 | 33343355 | The podocyte markers, nephrin and podocin, were down-regulated, while the mesenchymal markers, α-SMA and FSP-1, were up-regulated in DN mouse kidney; however, the changes in these markers were reversed on treatment with BSHX decoction. |
| 2407 | 33343355 | Together, our data demonstrated that BSHX decoction ameliorated renal function and podocyte epithelial-mesenchymal transition via inhibiting Rac1/PAK1/p38MAPK signaling pathway in high-fat diet/streptozotocin-induced diabetic mice. |
| 2408 | 33365127 | In the present study, the expression of TUG1, podocyte-specific markers (nephrin and podocin) and mitochondrial biogenesis-associated mRNAs (transcription factor A mitochondrial, cytochrome C oxidase subunit 5A and peroxisome proliferator-activated receptor γ coactivator 1α) were examined in urinary sediment of non-diabetic patients with biopsy-confirmed glomerulonephritides and healthy controls. |
| 2409 | 33537831 | Exogenous spermine attenuates diabetic kidney injury in rats by inhibiting AMPK/mTOR signaling pathway. |
| 2410 | 33537831 | The expression levels of podocyte marker proteins (nephrin, CD2‑associated protein and podocin) and autophagy‑related proteins [autophagy protein 5, microtube‑associated proteins 1A/1B light chain 3 (LC3)II/LC3I, Beclin 1 and phosphorylated (p)‑AMPK] were downregulated, while cleaved caspase‑3, P62 and p‑mTOR were increased. |
| 2411 | 33537831 | In conclusion, spermine may have the potential to prevent diabetic kidney injury in rats by promoting autophagy via regulating the AMPK/mTOR signaling pathway. |
| 2412 | 33671780 | It is an efficient endocrine regulator of the Renin-Angiotensin-Aldosterone System (RAAS) and erythropoiesis, exerts immunomodulatory effects, reduces the cardiovascular events and all-cause mortality. |
| 2413 | 33671780 | Moreover, Vitamin D major carrier, the D-binding protein (DBP), is less represented due to Nephrotic Syndrome (NS), proteinuria, and the alteration of the cubilin-megalin-amnionless receptor complex in the renal proximal tubule. |
| 2414 | 33671780 | Activated Vitamin D has been demonstrated to potentiate the antiproteinuric effect of RAAS inhibitors in IgA nephropathy and Lupus Nephritis, enforcing its role in the treatment of glomerulonephritis: calcitriol treatment, through Vitamin D receptor (VDR) action, can regulate the heparanase promoter activity and modulate the urokinase receptor (uPAR), guaranteeing podocyte preservation. |
| 2415 | 33671780 | It also controls the podocyte distribution by modulating mRNA synthesis and protein expression of nephrin and podocin. |
| 2416 | 33671780 | Paricalcitol demonstrated a significant role in suppressing RAAS genes expression: it significantly decreases angiotensinogen, renin, renin receptors, and vascular endothelial growth factor (VEGF) mRNA levels, thus reducing proteinuria and renal damage. |
| 2417 | 33733390 | Also described is a detailed immunofluorescence staining protocol to confirm successful differentiation using the podocyte-specific markers, Wilms' tumor protein (WT1) and podocin. |
| 2418 | 33970139 | Imaging of Podocytic Proteins Nephrin, Actin, and Podocin with Expansion Microscopy. |
| 2419 | 33970139 | Those adaptor proteins, such as podocin, link the backbone of the glomerular slit diaphragm, such as nephrin, to the actin cytoskeleton. |
| 2420 | 33970139 | The presented protocol enables the user to visualize actin, podocin, and nephrin in cells with super resolution imaging on a conventional microscope. |
| 2421 | 33970139 | Imaging of Podocytic Proteins Nephrin, Actin, and Podocin with Expansion Microscopy. |
| 2422 | 33970139 | Those adaptor proteins, such as podocin, link the backbone of the glomerular slit diaphragm, such as nephrin, to the actin cytoskeleton. |
| 2423 | 33970139 | The presented protocol enables the user to visualize actin, podocin, and nephrin in cells with super resolution imaging on a conventional microscope. |
| 2424 | 33970139 | Imaging of Podocytic Proteins Nephrin, Actin, and Podocin with Expansion Microscopy. |
| 2425 | 33970139 | Those adaptor proteins, such as podocin, link the backbone of the glomerular slit diaphragm, such as nephrin, to the actin cytoskeleton. |
| 2426 | 33970139 | The presented protocol enables the user to visualize actin, podocin, and nephrin in cells with super resolution imaging on a conventional microscope. |
| 2427 | 34168254 | Accelerated maturation in IL-6 newborns was suggested by early expression of podocyte-specific protein podocin in glomeruli, increased 5-methyl-cytosine (LC-MS analysis for CpG DNA methylation) and altered expression of certain genes of cell-cycle and apoptosis (RT-qPCR array-analysis). |
| 2428 | 34233930 | We analyzed the podocyte translatome in T2DN in podocin-Cre; Rosa26fsTRAP; eNOS-/-; db/db mice and compared it with that of streptozotocin-induced T1DN in podocin-Cre; Rosa26fsTRAP; eNOS-/- mice using translating ribosome affinity purification (TRAP) and RNA-seq. |
| 2429 | 34252407 | Our results showed that both Sar and insulin precluded the decreases of autophagy-related proteins (ATG5, Beclin1 and LC3B) and podocyte marker proteins (podocin, nephrin and synaptopodin) in the diabetic kidney. |
| 2430 | 34253875 | We showed that wogonin (4, 8, 16 μM) dose-dependently alleviated high glucose (HG)-induced MPC5 cell damage, accompanied by increased expression of WT-1, nephrin, and podocin proteins, and decreased expression of TNF-α, MCP-1, IL-1β as well as phosphorylated p65. |
| 2431 | 34253875 | Wogonin reversed HG-suppressed autophagy in MPC5 cells, evidenced by increased ATG7, LC3-II, and Beclin-1 protein, and decreased p62 protein. |
| 2432 | 34278447 | AS‑IV also reduced urinary albumin excretion, urinary albumin‑to‑creatinine ratio and creatinine clearance rate, as well as improved renal structural changes, accompanied by the upregulation of the podocyte markers podocin and synaptopodin. |
| 2433 | 34278447 | AS‑IV significantly inhibited the expression levels of NLRP3, caspase‑1 and IL‑1β in the renal cortex, and reduced the serum levels of tumor necrosis factor (TNF)‑α and monocyte chemoattractant protein‑1. |
| 2434 | 34288970 | Nephrin, KIRREL1, podocin, CD2AP, and TRPC6 are crucial members of the SD that interact with each other and contribute to the SD's structural and functional integrity. |
| 2435 | 34288970 | We found a diverse distribution of nephrin and KIRREL1 ranging from nematodes to higher vertebrates, whereas podocin, CD2AP, and TRPC6 are restricted to the vertebrates. |
| 2436 | 34288970 | Among invertebrates, nephrin and its orthologs consist of more immunoglobulin-3 domains, whereas in the vertebrates, CD80-like C2-set domains are predominant. |
| 2437 | 34288970 | Nephrin, KIRREL1, podocin, CD2AP, and TRPC6 are crucial members of the SD that interact with each other and contribute to the SD's structural and functional integrity. |
| 2438 | 34288970 | We found a diverse distribution of nephrin and KIRREL1 ranging from nematodes to higher vertebrates, whereas podocin, CD2AP, and TRPC6 are restricted to the vertebrates. |
| 2439 | 34288970 | Among invertebrates, nephrin and its orthologs consist of more immunoglobulin-3 domains, whereas in the vertebrates, CD80-like C2-set domains are predominant. |
| 2440 | 34387906 | Urine pellet (UP) mRNAs were assayed for podocyte (NPHS2/podocin and nephrin/NPHS1), distal tubule (aquaporin2), and profibrotic cytokine (TGFbeta1). |
| 2441 | 34441433 | The aim of this work was to identify genes involved in podocytes signaling and cytoskeletal regulation (NPHS1, NPHS2, SYNPO, WT1, TRPC6, GRM1, and NEUROD) in respect to glomerular pathology. |
| 2442 | 34575240 | Alpha-1 Acid Glycoprotein and Podocin mRNA as Novel Biomarkers for Early Glomerular Injury in Obese Children. |
| 2443 | 34596829 | WT-1, nephrin, podocin, E-cadherin, and α-SMA were determined by immunohistochemistry in the renal tissues of treated mice. |
| 2444 | 34596829 | It also increased the protein and mRNA levels of nephrin, podocin, and E-cadherin and decreased the expression of α-SMA in diabetic mice. |
| 2445 | 34596829 | The protein and mRNA expressions of TGF-β1, p-SMAD3, and kindlin-2 decreased in diabetic kidneys following triptolide treatment. |
| 2446 | 34596829 | The findings demonstrated that triptolide might protect podocytes during DN by inhibiting podocyte EMT through inactivation of kindlin-2, combined with the downregulation of P-SMAD3 in the TGF-β/Smad signaling pathway. |
| 2447 | 34596829 | WT-1, nephrin, podocin, E-cadherin, and α-SMA were determined by immunohistochemistry in the renal tissues of treated mice. |
| 2448 | 34596829 | It also increased the protein and mRNA levels of nephrin, podocin, and E-cadherin and decreased the expression of α-SMA in diabetic mice. |
| 2449 | 34596829 | The protein and mRNA expressions of TGF-β1, p-SMAD3, and kindlin-2 decreased in diabetic kidneys following triptolide treatment. |
| 2450 | 34596829 | The findings demonstrated that triptolide might protect podocytes during DN by inhibiting podocyte EMT through inactivation of kindlin-2, combined with the downregulation of P-SMAD3 in the TGF-β/Smad signaling pathway. |
| 2451 | 34654837 | Crb2 is a cell polarity-related type I transmembrane protein expressed in the apical membrane of podocytes. |
| 2452 | 34654837 | The number of glomerular Wt1-positive cells and the expressions of Nphs2, Podxl, and Nphs1 were reduced in podocyte-specific Crb2 knockout mice compared to negative control mice. |
| 2453 | 34694755 | Diabetes was associated with increases in blood glucose level, 24-h urinary albumin excretion rate, glomerular basement membrane thickness, renal oxidative stress markers, and renal mRNA or protein expression of transforming growth factor-β1, fibronectin, collagen-IV, tumour necrosis factor-α and vascular endothelial growth factor-A. |
| 2454 | 34694755 | Moreover, the expression of nephrin and podocin, and the mRNA expression of matrix metalloproteinase-9 were decreased in the diabetic group. |
| 2455 | 34780752 | In fructose-exposed conditionally immortalized human podocytes, we found that atractylodin inhibited podocyte hypermotility, and up-regulated slit diaphragm proteins podocin and nephrin, and cytoskeleton protein CD2-associated protein (CD2AP), α-Actinin-4 and synaptopodin expression, which were consistent with its anti-oxidative activity evidenced by up-regulation of catalase (CAT) and superoxide dismutase (SOD) 1 expression, and reduction of reactive oxygen species (ROS) production. |
| 2456 | 34780752 | Atractylodin also significantly suppressed expression of transient receptor potential channels 6 (TRPC6) and phosphorylated Ca2+/calmodulin-dependent protein kinase IV (CaMK4) in cultured podocytes with fructose exposure. |
| 2457 | 34780752 | Additionally, in fructose-exposed podocytes, CaMK4 siRNA up-regulated synaptopodin and reduced podocyte hypermotility, whereas, silencing of TRPC6 by siRNA decreased p-CaMK4 expression, inhibited podocyte hypermotility, showing TRPC6/p-CaMK4 signaling activation in podocyte hypermotility under fructose condition. |
| 2458 | 34780752 | These results first demonstrated that the anti-oxidative property of atractylodin may contribute to the suppression of podocyte hypermotility via inhibiting TRPC6/p-CaMK4 signaling and restoring synaptopodin expression abnormality. |
| 2459 | 34857869 | Co-cultured using a magnetic spheroid formation approach, conditionally immortalised (CI) human podocytes and glomerular endothelial cells (GEnCs) deposited mature, organized isoforms of collagen IV and Laminin. |
| 2460 | 34857869 | We demonstrate a dramatic upregulation of key podocyte (podocin, nephrin and podocalyxin) and GEnC (pecam-1) markers. |
| 2461 | 35086056 | Podocyte protection by Angptl3 knockout via inhibiting ROS/GRP78 pathway in LPS-induced acute kidney injury. |
| 2462 | 35086056 | Then, the changes in renal function, podocyte apoptosis, inflammatory factors (tumor necrosis factor-α, TNF-α; interleukin-6, IL-6; and interleukin-1β, IL-1β), reactive oxygen species (ROS), and endoplasmic reticulum (ER) stress were measured. |
| 2463 | 35086056 | Angptl3 knockout was associated with the (1) downregulation of Bax and upregulation of Bcl-2; (2) amelioration of the abnormal expression of nephrin, podocin, and CD2AP; (3) reduced ER stress; (4) reduced secretions of TNF-α, IL-6, and IL-1β; and (5) regulation of Bax expression via the ROS-related ER stress pathway. |
| 2464 | 35086056 | Our findings revealed that Angptl3 knockout alleviated the apoptosis of podocytes by regulating the ROS/GRP78 signaling pathway. |
| 2465 | 35102914 | Our aim was to assess the expression of podocyte-associated nephrin, podocin, and vascular endothelial growth factor (VEGF) A and their relation to renal function, proteinuria, and clinical outcome in patients with newly diagnosed multiple myeloma. |
| 2466 | 35102914 | Podocytes were identified by PCR tagging nephrin, podocin, and VEGF-A. |
| 2467 | 35102914 | Comparing to baseline urinary nephrin/creatinine, podocin/creatinine, VEGF-A/creatinine were significantly increased (P = 0.039, P = 0.001, P = 0.001 respectively) while renal function and proteinuria were improved in patients. |
| 2468 | 35102914 | Our aim was to assess the expression of podocyte-associated nephrin, podocin, and vascular endothelial growth factor (VEGF) A and their relation to renal function, proteinuria, and clinical outcome in patients with newly diagnosed multiple myeloma. |
| 2469 | 35102914 | Podocytes were identified by PCR tagging nephrin, podocin, and VEGF-A. |
| 2470 | 35102914 | Comparing to baseline urinary nephrin/creatinine, podocin/creatinine, VEGF-A/creatinine were significantly increased (P = 0.039, P = 0.001, P = 0.001 respectively) while renal function and proteinuria were improved in patients. |
| 2471 | 35102914 | Our aim was to assess the expression of podocyte-associated nephrin, podocin, and vascular endothelial growth factor (VEGF) A and their relation to renal function, proteinuria, and clinical outcome in patients with newly diagnosed multiple myeloma. |
| 2472 | 35102914 | Podocytes were identified by PCR tagging nephrin, podocin, and VEGF-A. |
| 2473 | 35102914 | Comparing to baseline urinary nephrin/creatinine, podocin/creatinine, VEGF-A/creatinine were significantly increased (P = 0.039, P = 0.001, P = 0.001 respectively) while renal function and proteinuria were improved in patients. |
| 2474 | 35126185 | Serum and glucocorticoid-inducible kinase 3 (SGK3) is involved in maintaining podocyte function by regulating the protein levels of podocin and CD2-associated protein. |
| 2475 | 35126185 | Nephrin is also one of the slit diaphragm proteins of podocytes, but whether SGK3 participates in podocyte injury by regulating the levels of nephrin remains unclear. |
| 2476 | 35126185 | In this study, we focused on whether SGK3 affects nephrin levels and the mechanisms involved in the same. |
| 2477 | 35126185 | In the kidneys of adriamycin (ADR)-induced podocyte injury mouse model, the protein levels of SGK3 and nephrin were significantly decreased. |
| 2478 | 35126185 | In ADR-treated conditionally immortalized mouse podocyte cells (MPCs), the protein levels of nephrin and SGK3 were inhibited, while the constitutive expression of SGK3 reversed the ADR-induced decline in nephrin protein levels. |
| 2479 | 35126185 | Furthermore, ADR treatment or SGK3 inactivation enhanced the ubiquitin-proteasome degradation of nephrin in MPCs, and dramatically activated downstream effector proteins of SGK3, neural precursor cells expressing developmentally downregulated protein 4 subtype 2 (Nedd4-2) and glycogen synthase kinase-3 β (GSK3β). |
| 2480 | 35126185 | Similarly, Nedd4-2 or GSK3β overexpression resulted in increased activity of Nedd4-2 or GSK3β, and significantly downregulated nephrin levels. |
| 2481 | 35126185 | Interestingly, ubiquitin-mediated protein degradation of nephrin was regulated by Nedd4-2, rather than by GSK3β. |
| 2482 | 35126185 | In summary, SGK3 inactivation downregulated the levels of nephrin by increasing Nedd4-2 and GSK3β activity in ADR-induced podocyte injury model; in particular, the SGK3/Nedd4-2 signaling pathway was found to be involved in ubiquitin-mediated proteasome degradation of nephrin. |
| 2483 | 35222021 | Effects of Shenkang Pills on Early-Stage Diabetic Nephropathy in db/db Mice via Inhibiting AURKB/RacGAP1/RhoA Signaling Pathway. |
| 2484 | 35222021 | In addition, SKP protected podocytes from injury by increasing nephrin and podocin expression. |
| 2485 | 35222021 | Weighted gene co-expression network analysis and network pharmacology analysis indicated that aurora kinase B (AURKB), Rac GTPase activating protein 1 (RacGAP1) and SHC binding, and spindle associated 1 (shcbp1) might be the core targets of SKP. |
| 2486 | 35222021 | The mechanism may involve down-regulation of the AURKB/RacGAP1/RhoA pathway. |
| 2487 | 35277865 | Hirudin also attenuated cytoskeletal protein (synaptopodin, nephrin, and podocin) disruption, ERS activation, and apoptosis in PAN mice and PAN-induced podocytes. |
| 2488 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2489 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2490 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2491 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2492 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2493 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2494 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2495 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2496 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2497 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2498 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2499 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2500 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2501 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2502 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2503 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2504 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2505 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2506 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2507 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2508 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2509 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2510 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2511 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2512 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2513 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2514 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2515 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2516 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2517 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2518 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2519 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2520 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2521 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2522 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2523 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2524 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2525 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2526 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2527 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2528 | 23657570 | Opposing effects of podocin on the gating of podocyte TRPC6 channels evoked by membrane stretch or diacylglycerol. |
| 2529 | 23657570 | Gain-of-function mutations in the transient receptor potential (TRP) cation channel subfamily C member 6 (TRPC6) gene and mutations in the NPHS2 gene encoding podocin result in nephrotic syndromes. |
| 2530 | 23657570 | Stretch activation of podocyte TRPC6 persisted in the presence of inhibitors of phospholipase C (U-73122) and phospholipase A2 (ONO-RS-082). |
| 2531 | 23657570 | Podocin and TRPC6 interact at their respective COOH termini. |
| 2532 | 23657570 | Knockdown of podocin markedly increased stretch-evoked activation of TRPC6 but nearly abolished TRPC6 activation evoked by a diacylglycerol analog. |
| 2533 | 23657570 | These data suggest that podocin acts as a switch to determine the preferred mode of TRPC6 activation. |
| 2534 | 23657570 | They also suggest that podocin deficiencies will result in Ca(2+) overload in foot processes, as with gain-of-function mutations in the TRPC6 gene. |
| 2535 | 23657570 | Finally, they suggest that mechanical activation of TRP family channels and the preferred mode of TRP channel activation may depend on whether members of the stomatin/prohibitin family of hairpin loop proteins are present. |
| 2536 | 29270765 | Given our finding that maxacalcitol does not repress renin, the reduction of proteinuria by this agent is likely due to direct upregulation of the nephrin and podocin in podocytes. |
| 2537 | 29270765 | Moreover, this agent downregulates the mesenchymal marker desmin in podocytes and blocks transforming growth factor-beta autoinduction, leading to attenuation of renal fibrosis in a unilateral ureteral obstructive (UUO) model. |
| 2538 | 22828802 | This effect of NMDA was associated with increased cell-surface expression of p47(phox), a cytosolic regulatory subunit of the NADPH oxidase NOX2. |
| 2539 | 22828802 | NMDA treatment also evoked robust activation of Rho but not Rac,consistent with previous studies of downstream effectors of TRPC6 activation. |
| 2540 | 22828802 | Exposing cells to NMDA for 24 h reduced total and cell surface expression of the podocyte markers nephrin and podocin, but there was no loss of cells. |
| 2541 | 22828802 | With longer NMDA exposure (72 h), we observed loss of cells associated with nuclear fragmentation and increased expression of caspase-3, caspase-6, and Bax, suggesting an apoptotic process. |