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Gene Information
Gene symbol: ACTC1
Gene name: actin, alpha, cardiac muscle 1
HGNC ID: 143
Synonyms: CMD1R
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 34497508 | Additionally, the elevated expressions of collagen and α-smooth muscle actin (α-SMA) in the kidney from db/db mice were found to be significantly suppressed after DL-NBP treatment. |
| 2 | 34497508 | Moreover, we found that DL-NBP could not only reduce the endoplasmic reticulum stress (ERS), but also suppress activation of the renin-angiotensin system to inhibit vascular endothelial growth factor (VEGF) level, which subsequently reduces the podocyte apoptosis in kidney of db/db mice. |
| 3 | 34308664 | Higher expression of transforming growth factor-βR1 and β-catenin and suppressed expression of carnitine palmitoyltransferase 1A in nephrin-positive cells were found in the kidneys of diabetic GRPKO mice. |
| 4 | 34308664 | Moreover, endothelial cells treated with conditioned media from podocytes lacking GR showed increased expression of α-smooth muscle actin, transforming growth factor-βR1 and β-catenin levels. |
| 5 | 33901627 | Meanwhile, C-peptide suppressed high glucose-induced epithelial-mesenchymal transition (EMT) and renal fibrosis via decreasing the expression of snail, vimentin, α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF). |
| 6 | 33901627 | Moreover, the Notch and transforming growth factor-β (TGF-β) signaling pathways were activated by high glucose, and treatment with C-peptide down-regulated the expression of the Notch signaling molecules Notch 1 and Jagged 1 and the TGF-β signaling molecule TGF-β1. |
| 7 | 32691413 | Thus, in this study, the role of miR-27a-3p-prohibitin/TMBIM6 signaling axis in the progression of DN was elucidated. |
| 8 | 32691413 | Our results showed that miR-27a-3p was upregulated and prohibitin or transmembrane BAX inhibitor motif containing 6 (TMBIM6) was downregulated in the kidney tissues of db/db mice and HG-treated HK-2 cells. |
| 9 | 32691413 | Silencing miR-27a-3p enhanced the expression of prohibitin and TMBIM6 in the kidney tissues and HK-2 cells. |
| 10 | 32691413 | MiR-27a-3p silencing ameliorated renal fibrosis, reflected by reduced profibrogenic genes (e.g., transforming growth factor β1, fibronectin, collagen I and III, and α-smooth muscle actin). |
| 11 | 32691413 | In addition, miR-27a-3p silencing attenuated endoplasmic reticulum (ER) stress, reflected by reduced expression of p-IRE1α, p-eIF2α, XBP1s, and CHOP. |
| 12 | 32691413 | Mechanically, we identified prohibitin and TMBIM6 as direct targets of miR-27a-3p. |
| 13 | 32691413 | Inhibition of miR-27a-3p protected HG-treated HK-2 cells from apoptosis, extracellular matrix accumulation, mitochondrial dysfunction, and ER stress by regulating prohibitin or TMBIM6. |
| 14 | 32691413 | Taken together, we reveal that miR-27a-3p-prohibitin/TMBIM6 signaling axis regulates the progression of DN, which can be a potential therapeutic target. |
| 15 | 32451085 | TGF-β1 decreased the expression of epithelial markers such as nephrin, zonula occludens-1 (ZO-1), while it increased the mesenchymal markers, including fibronectin (FN), vimentin, and α-smooth muscle actin (α-SMA) in the podocytes. |
| 16 | 31720047 | MSCs also prevented podocyte damage and renal fibrosis by decreasing the expression of fibronectin, collagen 1α1, and α-smooth muscle actin. |
| 17 | 31377057 | Inhibition of the ERK1/2-mTORC1 axis ameliorates proteinuria and the fibrogenic action of transforming growth factor-β in Adriamycin-induced glomerulosclerosis. |
| 18 | 31377057 | Here, we identified the regulation of mammalian target of rapamycin complex1 (mTORC1) by TGF-β via ERK1/2 in the Adriamycin-induced murine model of focal segmental glomerulosclerosis. |
| 19 | 31377057 | Phosphorylation of the TGF-β receptor-I (TGF-βRI), Smad3, ERK1/2 and ribosomal protein S6 were evident in the glomeruli of adriamycin-treated mice. |
| 20 | 31377057 | Targeting TGFβ-RI and mTORC1 with pharmacological inhibitors suppressed TGF-β signaling in glomeruli and significantly reduced albuminuria, glomerulosclerosis, protein levels of collagen 4α3, plasminogen activator inhibitor-1, and vimentin and restored mRNA levels of podocyte markers. |
| 21 | 31377057 | Low dose US Food and Drug Administration (FDA)-approved MEK/ERK inhibitor trametinib/GSK1120212 blunted TGF-β1-induced mTORC1 activation in podocytes, ameliorated up-regulation of TGF-β, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, fibronectin and α-smooth muscle actin and prevented albuminuria and glomerulosclerosis with improved serum albumin. |
| 22 | 31377057 | In cultured podocytes, this pathway was found to be associated with translation of fibrogenic collagen 4α3 and plasminogen activator inhibitor-1, without influencing their transcription. |
| 23 | 30811433 | Differential trafficking of albumin and IgG facilitated by the neonatal Fc receptor in podocytes in vitro and in vivo. |
| 24 | 30811433 | In other epithelial cells, the neonatal Fc receptor (FcRn) is required to salvage albumin and IgG from the degradative pathway thereby allowing these proteins to be transcytosed or recycled. |
| 25 | 30811433 | Here we directly examine the role of FcRn in albumin and IgG trafficking in podocytes by studying handling of these proteins in FcRn knockout (KO) podocytes in vitro and in a podocyte-specific FcRn knockout mice in vivo. |
| 26 | 30811433 | In vitro, we find that knockout of FcRn leads to IgG accumulation in podocytes but does not alter albumin trafficking. |
| 27 | 30811433 | Similarly, in vivo, podocyte-specific knockout of FcRn does not result in albumin accumulation in podocytes in vivo as measured by mean albumin fluorescence intensity whereas these mice demonstrate significant intraglomerular accumulation of IgG over time. |
| 28 | 30811433 | In addition we find that podocyte-specific FcRn KO mice demonstrate mesangial expansion as they age and activation of mesangial cells as demonstrated by increased expression of α-smooth muscle actin. |
| 29 | 30201496 | At the margins of crescents Sox9+/Pax8+ cells additionally expressed podocyte markers. |
| 30 | 30201496 | In contrast, in sclerotic lesions a minority of Sox9+/Pax8+ cells expressed the myofibroblast marker α-smooth muscle actin. |
| 31 | 30201496 | In glomerular Sox9+ cells Jagged 1 was up-regulated. |
| 32 | 30132344 | Downregulation of microRNA-429 contributes to angiotensin II-induced profibrotic effect in rat kidney. |
| 33 | 30132344 | The present study determined whether miR429 participated in angiotensin (ANG) II-induced EMT and fibrogenesis in renal cells. |
| 34 | 30132344 | In NRK-52E cells, a rat proximal tubular cell line, incubation of ANG II (10-9 M) for 24 h significantly reduced the level of miR429 by 60% and increased the protein levels of mesenchymal markers α-smooth muscle actin and fibroblast-specific protein-1 by threefold and decreased epithelial marker E-cadherin by 60%, which was blocked by losartan, an AT1 receptor antagonist. |
| 35 | 30132344 | In cells overexpressed with miR429 transgene, ANG II-induced increases in collagen were abolished. |
| 36 | 30132344 | Intrarenal transfection of lentivirus expressing miR429 also reversed the ANG II-induced changes in the EMT markers and collagen in the kidneys. |
| 37 | 30132344 | The ANG II-induced increase in urinary albumin was significantly inhibited by miR429 transgene. |
| 38 | 30054312 | Mesangial and tubule interstitial expression of the myofibroblast markers α-smooth muscle actin (α-SMA) and type IV collagen (Col-IV) was lower in HFD + AC261-treated mice compared with HFD alone. |
| 39 | 29909344 | Moreover, hesperetin repaired the function of podocyte by increasing renal nephrin expression and decreasing renal alpha-smooth muscle actin expression. |
| 40 | 29909344 | Furthermore, hesperetin inhibited the expression of transforming growth factor-β1 (TGF-β1) and its downstream effectors integrin-linked kinase (ILK) and Akt. |
| 41 | 29660398 | We performed an immunohistochemical study using a panel of endothelial, myoid, mesenchymal and stem/progenitor markers, namely CD31, CD34, CD105 (endoglin), CD117/c-kit, nestin, desmin, α-smooth muscle actin (α-SMA) and the heavy chain of smooth muscle myosin (SMM). |
| 42 | 29660398 | The capsular SC/TCs had a strong CD34 and partial nestin and CD105 immunopositivity. |
| 43 | 29660398 | Subcapsular and interstitial SC/TCs expressed c-kit, nestin, CD105, but also α-SMA and SMM, therefore having a myoid phenotype. |
| 44 | 29660398 | The endothelial SC/TCs phenotype was CD31+/CD34+/CD105+/nestin±/SMM±/α-SMA±. |
| 45 | 29660398 | In epithelial cells, we found a positive expression for CD31, CD117/c-kit, desmin, CD34, SMM, and CD105. |
| 46 | 29033543 | Moreover, ECH inhibited the TGF-β1/Smads signaling pathway, downregulated fibronectin (FN), collagen IV, and alpha-smooth muscle actin (α-SMA) levels, and upregulated E-cadherin level in the db/db mice model of DN. |
| 47 | 28739650 | We examined whether BMS002, a novel dual LPAR1 and LPAR3 antagonist, affects development of DN in endothelial nitric oxide synthase-knockout db/db mice. |
| 48 | 28739650 | LPAR inhibition also reduced histologic glomerular injury; decreased the expression of profibrotic and fibrotic components, including fibronectin, α-smooth muscle actin, connective tissue growth factor, collagen I, and TGF-β; and reduced renal macrophage infiltration and oxidative stress. |
| 49 | 28645189 | The potential role of retinoic acid receptor α on glomerulosclerosis in rats and podocytes injury is associated with the induction of MMP2 and MMP9. |
| 50 | 28645189 | Further experiments indicated that RARα inhibited the accumulation of TGF-β1, α-smooth muscle actin, collagen IV, and fibronectin, while it induced MMP2 and MMP9 excessive expression in podocytes in vitro. |
| 51 | 28645189 | RARα improved the renal function and attenuated the progression of GS that was associated with the over-expression of MMP2 and MMP9. |
| 52 | 28277542 | MicroRNA-27a promotes podocyte injury via PPARγ-mediated β-catenin activation in diabetic nephropathy. |
| 53 | 28277542 | MicroRNA-27a (miR-27a), peroxisome proliferator-activated receptor γ (PPARγ) and β-catenin pathways have been involved in the pathogenesis of DN. |
| 54 | 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. |
| 55 | 28063595 | However, SS-31 treatment reduced markers of parietal epithelial cell activation (Collagen IV, pERK1/2, and α-smooth muscle actin). |
| 56 | 27440779 | Additionally, markers of epithelial-to-mesenchymal transition (platelet-derived growth factor receptor-β, α-smooth muscle actin, Notch-3) and PEC activation (CD44, collagen IV) were further increased by mTOR reduction. |
| 57 | 26687735 | Preparation of PCKSs induced an inflammatory tissue response, whereas long-term incubation (96 hours) induced fibrogenesis as shown by an increased expression of collagen type 1A1 (COL1A1) and fibronectin 1 (FN1). |
| 58 | 26687735 | Moreover, TGF-β1 exposure augmented fibrosis, as illustrated by an increased expression of multiple fibrosis markers including COL1A1, FN1, and α-smooth muscle actin. |
| 59 | 26673167 | In addition to increasing creatinine clearance, Tongxinluo decreased urinary albumin excretion, oxidative stress injury markers including malondialdehyde and protein carbonyls, and expression of nicotinamide adenine dinucleotide phosphate oxidase subunits and its activity in SHR kidneys. |
| 60 | 26673167 | While decreasing phosphorylation of FoxO1, Tongxinluo also inhibited the phosphorylation of extracellular signal-regulated kinase1/2 and p38 and enhanced manganese superoxide dismutase and catalase activities in SHR kidneys. |
| 61 | 26673167 | Furthermore, histology revealed attenuation of glomerulosclerosis and renal podocyte injury, while Tongxinluo decreased the expression of α-smooth muscle actin, extracellular matrixprotein, transforming growth factor β1 and small mothers against decapentaplegic homolog 3,and improved tubulointerstitial fibrosis in SHR kidneys. |
| 62 | 26673167 | Finally, Tongxinluo inhibited inflammatory cell infiltration as well as expression of tumor necrosis factor-α and interleukin-6. |
| 63 | 26552047 | Furthermore, NOX2TG-Akita mice exhibited distinct phenotypic changes in glomerular mesangial cells expressing α-smooth muscle actin, and in podocytes expressing increased levels of desmin, whereas the glomeruli generated increased levels of ROS. |
| 64 | 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. |
| 65 | 25736988 | PI3K/Akt pathway is involved in the progression of DN. |
| 66 | 25736988 | In the present study, we demonstrated that PI3K/Akt pathway was activated in podocytes exposed to high glucose conditions, accompanied by down-regulation of the podocalyxin (PCX) and nephrin expression and up-regulation of the desmin and α-smooth muscle actin (α-SMA) expression. |
| 67 | 25736988 | Inhibition of PI3K/Akt pathway by chemical LY294002 or Phosphase and tensin homology deleted on chromosome ten (PTEN) prevented the phenotypic transition. |
| 68 | 25736988 | These findings indicate that PTEN/PI3K/Akt pathway mediates high glucose-induced phenotypic transition in podocytes. |
| 69 | 25661065 | Recent studies have shown that microRNA (miR)-346 regulates the expression of glycogen synthase kinase (GSK)-3β and activates the Wnt/β-catenin pathway, which regulates the differentiation of human bone marrow mesenchymal stem cells. |
| 70 | 25661065 | Podocytes were transfected with miR-346 mimic or miR-346 inhibitor to test whether miR-346 affected the expression of nephrin, α-smooth muscle actin (α-SMA), and GSK-3β. |
| 71 | 25651362 | In Dicer1-null renal stromal cells, expression of factors associated with migration, proliferation, and morphogenic functions including α-smooth muscle actin, integrin-α8, -β1, and the WNT pathway transcriptional regulator LEF1 were reduced. |
| 72 | 25071087 | Here, we show that β-catenin triggers ubiquitin-mediated protein degradation of Wilms' tumor 1 (WT1) and functionally antagonizes its action. |
| 73 | 25071087 | This change in WT1/β-catenin ratio was accompanied by loss of podocyte-specific nephrin, podocalyxin, and synaptopodin and acquisition of mesenchymal markers Snail1, α-smooth muscle actin, and fibroblast-specific protein 1. |
| 74 | 25071087 | In vitro, overexpression of β-catenin induced WT1 protein degradation through the ubiquitin proteasomal pathway, which was blocked by MG-132. |
| 75 | 25071087 | WT1 and β-catenin also competed for binding to common transcriptional coactivator CREB-binding protein and mutually repressed the expression of their respective target genes. |
| 76 | 25071087 | In glomerular miniorgan culture, activation of β-catenin by Wnt3a repressed WT1 and its target gene expression. |
| 77 | 25071087 | In vivo, blockade of Wnt/β-catenin signaling by endogenous antagonist Klotho induced WT1 and restored podocyte integrity in adriamycin nephropathy. |
| 78 | 25071087 | These results show that β-catenin specifically targets WT1 for ubiquitin-mediated degradation, leading to podocyte dedifferentiation and mesenchymal transition. |
| 79 | 25071087 | Our data also suggest that WT1 and β-catenin have opposing roles in podocyte biology, and that the ratio of their expression levels dictates the state of podocyte health and disease in vivo. |
| 80 | 24371298 | In cultured mouse podocytes, ET-1 caused loss of the podocyte differentiation marker synaptopodin and acquisition of the mesenchymal marker α-smooth muscle actin. |
| 81 | 24371298 | Activated ET(A)R recruited β-arrestin-1 to form a trimeric complex with Src leading to epithelial growth factor receptor (EGFR) transactivation and β-catenin phosphorylation, which promoted gene transcription of Snail. |
| 82 | 23859838 | The expression of alpha-smooth muscle actin (α-SMA), proliferating cell nuclear antigen (PCNA) and transforming growth factor-beta1 (TGF-β1) in the kidney was examined by immunohistochemical staining and western blot analysis. |
| 83 | 23447065 | Hyperplastic epithelium was negative for genetic podocyte tags, but positive for the parietal epithelial cell marker claudin-1, and expressed Notch1, Jagged1, and Hes1 mRNA and protein. |
| 84 | 23447065 | Enhanced Notch mRNA expression induced by transforming growth factor-β1 in cultured parietal epithelial cells was associated with mesenchymal markers (α-smooth muscle actin, vimentin, and Snail1). |
| 85 | 22484642 | These floating cells were immunohistologically identified as podocytes, by the expression of podocalyxin, vimentin, Wilms' tumor 1, synaptopodin and nephrin with positivities of 100%, 88.4%, 80.4%, 74.7% and 22.6%, respectively. |
| 86 | 22484642 | Immunostaining of both detached and capillary-attached podocytes for Bax, Bcl-2, desmin, fibroblast-specific protein-1, α-smooth muscle actin and Ki-67 was negative, as were TUNEL assays. |
| 87 | 21997392 | Compared with normal glomeruli, fewer cells stained for APOL1 in FSGS and HIVAN glomeruli, even when expression of the podocyte markers GLEPP1 and synaptopodin appeared normal. |
| 88 | 21997392 | Unexpectedly, in both FSGS and HIVAN but not normal kidneys, the media of medium artery and arterioles contained a subset of α-smooth muscle actin-positive cells that stained for APOL1. |
| 89 | 21704028 | The study determines the effect of genistein on inflammatory status and expression of nuclear factor-kappa B (NF-κB p65), transforming growth factor-β1 (TGF-β1) and receptor for advanced glycation end products (RAGE) in kidney of fructose-fed rats. |
| 90 | 21704028 | The expression of NF-κB P(65), TGF-β1 and RAGE, histochemical localization of α-smooth muscle actin (α-SMA), levels of tumour necrosis factor-α (TNF-α) and interleukin-6(IL-6) and ultrastructural analysis were performed at the end of the experimental period. |
| 91 | 21691087 | It was found that Hcys induced significant EMT in podocytes, as shown by marked decreases in slit diaphragm-associated protein P-cadherin and zonula occludens-1 as epithelial markers and by dramatic increases in the expression of mesenchymal markers, fibroblast specific protein-1 and α-smooth muscle actin, which were detected by all examinations via immunocytochemistry, real time RT-PCR and Western blot analysis. |
| 92 | 21691087 | In addition, NADPH oxidase subunit, gp91(phox) and GH receptors aggregated in membrane raft clusters, which produced O(2).(-) in response to Hcys and could be blocked by GH, membrane raft disruptors filipin and MCD or NADPH oxidase inhibitor, apocynin. |
| 93 | 21647593 | The present study tested the hypothesis that hyperhomocysteinemia (hHcys) induces podocytes to undergo epithelial-to-mesenchymal transition (EMT) through the activation of NADPH oxidase (Nox). |
| 94 | 21647593 | It was found that increased homocysteine (Hcys) level suppressed the expression of slit diaphragm-associated proteins, P-cadherin and zonula occludens-1 (ZO-1), in conditionally immortalized mouse podocytes, indicating the loss of their epithelial features. |
| 95 | 21647593 | Meanwhile, Hcys remarkably increased the abundance of mesenchymal markers, such as fibroblast specific protein-1 (FSP-1) and α-smooth muscle actin (α-SMA). |
| 96 | 21647593 | In mice lacking gp91( phox ) (gp91(-/-)), an essential Nox subunit gene, hHcys-enhanced podocyte EMT and consequent glomerular injury were examined. |
| 97 | 21440751 | For this purpose we evaluated the vinculin- and paxillin-containing adhesion complexes and α-smooth muscle actin (α-SMA) expression on tubular cells and glomerular podocytes in first year renal allograft biopsy specimens of 74 patients. |
| 98 | 20818613 | To identify morphological and developmental changes in protein and RNA expression patterns during nephrogenesis, immunohistochemistry and quantitative real-time PCR were used to assess temporal and spatial expression of WT1, Pax2, Nestin, Synaptopodin, alpha-smooth muscle actin (α-SMA), CD31, vascular endothelial growth factor (VEGF), and Gremlin. |
| 99 | 20818613 | Mature podocytes expressing WT1, Nestin, and Synaptopodin were observed from the mid-third trimester through adulthood. |
| 100 | 20818613 | The developing glomerulus was positive for α-SMA (vascular smooth muscle) and Gremlin (mesangial cells), CD31 (glomerular endothelium), and VEGF (endothelium), and showed loss of expression of these markers as glomerular maturation was completed. |
| 101 | 20518888 | Sections were immunostained for nestin, alpha-smooth muscle actin (alpha-SMA), desmin, vimentin, CD34, and other stromal markers. |
| 102 | 20518888 | Interestingly, we observed a concomitant appearance of nestin- and CD34-positive myofibroblasts under fibrosing conditions. |
| 103 | 20505657 | ILK expression was induced in mouse podocytes by various injurious stimuli known to cause proteinuria including TGF-beta1, adriamycin, puromycin, and high ambient glucose. |
| 104 | 20505657 | Ectopic expression of ILK in podocytes decreased levels of the epithelial markers nephrin and ZO-1, induced mesenchymal markers such as desmin, fibronectin, matrix metalloproteinase-9 (MMP-9), and alpha-smooth muscle actin (alpha-SMA), promoted cell migration, and increased the paracellular albumin flux across podocyte monolayers. |
| 105 | 20505657 | ILK also induced Snail, a key transcription factor mediating epithelial-mesenchymal transition (EMT). |
| 106 | 20505657 | Blockade of ILK activity with a highly selective small molecule inhibitor reduced Snail induction and preserved podocyte phenotypes following TGF-beta1 or adriamycin stimulation. |
| 107 | 20505657 | In vivo, this ILK inhibitor ameliorated albuminuria, repressed glomerular induction of MMP-9 and alpha-SMA, and preserved nephrin expression in murine adriamycin nephropathy. |
| 108 | 20505657 | Our results show that upregulation of ILK is a convergent pathway leading to podocyte EMT, migration, and dysfunction. |
| 109 | 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. |
| 110 | 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. |
| 111 | 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. |
| 112 | 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. |
| 113 | 18268475 | We investigated whether the intermediate filament protein and neural stem cell marker nestin characterizes the glomerular progenitor/reserve cell population immigrating the glomerulus after mesangial cell (MC) injury in the rat (anti-Thy1 nephritis). |
| 114 | 18268475 | At the peak of mesangial proliferation and expansion (day 5) most OX-7-positive MCs expressed nestin largely colocalizing with the activation marker alpha-smooth muscle actin and the proliferation marker PCNA. |
| 115 | 17464107 | In order to determine the characteristics of human glomerular development, we investigated the process of glomerular development by staining fetal and infant kidneys for CD31, CD34 and FB21, markers for endothelial cells, alpha-smooth muscle actin (alpha-SMA), a marker for mesangial cells, and nephrin, a marker for podocytes. |
| 116 | 17464107 | In each group, glomerular development was classified according to the developmental stage and the staining patterns for CD31, CD34, FB21, alpha-SMA and nephrin. |
| 117 | 17464107 | The staining patterns for CD31, CD34 and FB21 were similar in endothelial cells after 25 weeks of gestation. |
| 118 | 17267748 | Aside from the delay in podocyte maturation, DDS glomeruli show swollen endothelial cells, reminiscent of endotheliosis, together with incompletely fused capillary basement membranes; a dramatic decrease in collagen alpha4(IV) and laminin beta2 chains; and the presence of immature or activated mesangial cells that express alpha-smooth muscle actin. |
| 119 | 17210924 | We investigated nestin expression in human adult and fetal kidney as well as CDK5 presence in adult human podocytes. |
| 120 | 17210924 | Confocal microscopy demonstrated that adult glomeruli display nestin immunoreactivity in vimentin-expressing cells with the podocyte morphology and not in cells bearing the endothelial marker CD31. |
| 121 | 17210924 | Glomerular nestin-positive cells were CDK5 immunoreactive as well. |
| 122 | 17210924 | Similar experiments carried out with antibodies raised against nestin and alpha-smooth muscle actin showed that the first mesangial cells that populate the developing glomeruli expressed nestin. |
| 123 | 17137212 | Using an immunoenzyme method, we examined eleven biopsy samples from patients with hypertensive nephrosclerosis for two synthetic and secreting phenotypes, a-smooth muscle actin (alpha-SMA) and collagen type III (Col. |
| 124 | 16938652 | At 4 days, the cells altered their phenotype, as shown by a change in shape, an increase in intracellular staining for alpha-smooth muscle actin (alpha-SMA), a decrease in membrane staining for cytokeratin, and an increase in matrix deposition. |
| 125 | 16938652 | Changing the medium after 4 days by excluding TGF-beta(1) and adding fetal bovine serum (FBS) [as a source of epidermal growth factor (EGF) and other growth factors] caused the cells to revert to their original epithelial phenotype. |
| 126 | 16938652 | Staining the cells for expression of EGF receptor before and after exposure to TGF-beta(1) caused this receptor, originally present on the plasma membrane, to become partly intracellular after 4 days of TGF-beta(1) exposure and completely intracellular after 8 days of TGF-beta(1) exposure. |
| 127 | 16938652 | It seems that TGF-beta(1) exposure progressively downregulates the EGF receptor on the membrane, rendering the cell refractory to EGF signals critical for maintaining the epithelial phenotype. |
| 128 | 16938651 | TGF-beta1 and integrin synergistically facilitate the differentiation of rat podocytes by increasing alpha-smooth muscle actin expression. |
| 129 | 16938651 | TGF-beta1 and integrin synergistically facilitate the differentiation of rat podocytes by increasing alpha-smooth muscle actin expression. |
| 130 | 16938651 | This study was designed to identify whether podocytes can differentiate by the expression of alpha-smooth muscle actin (alpha-SMA), under the effects of TGF-beta(1) (transforming growth factor-beta(1)) and integrin. |
| 131 | 16938651 | This study was designed to identify whether podocytes can differentiate by the expression of alpha-smooth muscle actin (alpha-SMA), under the effects of TGF-beta(1) (transforming growth factor-beta(1)) and integrin. |
| 132 | 16938651 | The addition of calphostin [inhibitor of protein kinase C (PKC)] and genistein [inhibitor of focal adhesion kinase (FAK)] also decreased the expression of alpha-SMA protein and the percentage of alpha-SMA positive cells stimulated by TGF-beta(1) (both P < 0.01). |
| 133 | 16938651 | The addition of calphostin [inhibitor of protein kinase C (PKC)] and genistein [inhibitor of focal adhesion kinase (FAK)] also decreased the expression of alpha-SMA protein and the percentage of alpha-SMA positive cells stimulated by TGF-beta(1) (both P < 0.01). |
| 134 | 16510766 | Eight weeks after disease induction, anti-PDGF-D therapy significantly ameliorated focal segmental glomerulosclerosis, podocyte damage (de novo desmin expression), tubulointerstitial damage, and fibrosis as well as the accumulation of renal interstitial matrix including type III collagen and fibronectin. |
| 135 | 16510766 | Treatment with anti-PDGF-D also reduced the cortical infiltration of monocytes/macrophages on day 56, possibly related to lower renal cortical complement activation (C5b-9 deposition) and/or reduced epithelial-to-mesenchymal transition (preserved cortical expression of E-cadherin and reduced expression of vimentin and alpha-smooth muscle actin). |
| 136 | 12955485 | Insulin-like growth factor binding protein-2 modulates podocyte mitogenesis. |
| 137 | 12955485 | To study the role of insulin-like growth factors (IGF) in podocyte maturation, we isolated and characterized fetal visceral glomerular epithelial cells from human kidneys obtained at 8-18 weeks gestation. |
| 138 | 12955485 | Cells were identified as podocyte lineage by their cobblestone morphology and immunoreactivity with synaptopodin, Wilms tumor-1 suppressor gene product (WT-1), complement receptor CR1, and cytoskeletal proteins smooth muscle actin and vimentin. |
| 139 | 12955485 | Stimulation of the podocyte cell monolayers with IGF-II resulted in a slight increase in mitogenesis, an effect that was concentration and time dependent and abrogated by co-incubation with exogenous IGF binding protein 2 (IGFBP-2). |
| 140 | 12955485 | IGF-II stimulation enhanced IGFBP-2 production in a dose- and time-dependent fashion and was associated with an increase in IGFBP-2 mRNA production. |
| 141 | 12955485 | These data demonstrate that IGF-II-stimulated IGFBP-2 production appears to inhibit the mitogenic effect of IGF-II, and may have an autocrine effect on the maturation, differentiation, and survival of fetal podocytes. |
| 142 | 11228169 | Immunohistochemical studies showed increased fibronectin and desmin expression in glomeruli and tubulointerstitium and increased vimentin and alpha-smooth muscle actin in the tubulointerstitial area from the renal cortex of RT18 rats (P: < 0.05). |
| 143 | 10482316 | Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes. |
| 144 | 10482316 | Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously. |
| 145 | 10482316 | The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin. |
| 146 | 9773782 | In all of the healthy subjects and all of the patients except those with PGN (disease control subjects), VPF/VEGF protein and mRNA were detected mainly in podocytes. |
| 147 | 9773782 | However, in some PGN patients, VPF/VEGF protein was demonstrated clearly in MC as well as in podocytes, as some of the VPF/VEGF was colocalized with alpha-smooth muscle actin, a marker of activated MC, and VPF/VEGF mRNA was expressed by MC and podocytes. |
| 148 | 9773782 | The time between biopsy and disease onset was significantly shorter in PGN patients with than in those without mesangial VPF/VEGF expression (P < 0.01). |
| 149 | 8995738 | Cell injury in podocytes (evidenced as increased expression of desmin and by electron microscopy) and interstitial fibroblasts (increased expression of alpha-smooth muscle actin) and mild glomerular hypertrophy were witnessed as early as three to four months of age and preceded glomerulosclerosis and interstitial fibrosis. |
| 150 | 8995738 | Cell injury in podocytes (evidenced as increased expression of desmin and by electron microscopy) and interstitial fibroblasts (increased expression of alpha-smooth muscle actin) and mild glomerular hypertrophy were witnessed as early as three to four months of age and preceded glomerulosclerosis and interstitial fibrosis. |
| 151 | 8995738 | Only minor evidence of mesangial cell activation (as assessed by glomerular (de novo alpha-smooth muscle actin or type I collagen expression or increased cell proliferation) was noted throughout the observation period. |
| 152 | 8995738 | Only minor evidence of mesangial cell activation (as assessed by glomerular (de novo alpha-smooth muscle actin or type I collagen expression or increased cell proliferation) was noted throughout the observation period. |
| 153 | 8647942 | The cytoskeletal linking proteins, moesin and radixin, are upregulated by platelet-derived growth factor, but not basic fibroblast growth factor in experimental mesangial proliferative glomerulonephritis. |
| 154 | 8647942 | The expression of the two cytoskeletal linking proteins, moesin and radixin, was examined in experimental mesangial proliferative nephritis in rats (anti-Thy1 model). |
| 155 | 8647942 | Moesin and radixin mRNA and protein are constitutively expressed in all cell types of normal rat glomeruli, except podocytes. |
| 156 | 8647942 | In the anti-Thy1 model the expression of moesin and radixin was increased in infiltrating macrophages and in activated, alpha-smooth muscle actin-positive mesangial cells and was concentrated in the cellular extensions of mesangial cells in areas of glomerular remodelling. |
| 157 | 8647942 | Studies using neutralizing antibodies demonstrated that the increase in moesin and radixin expression by mesangial cells is mediated by PDGF, but not bFGF. |
| 158 | 8647942 | The increase in these cytoskeletal proteins appears to be regulated primarily (radixin) or partially (moesin) posttranscriptionally. |
| 159 | 8647942 | The data suggest that PDGF mediated upregulation of the cytoskeletal proteins, moesin and radixin, is important for cell migration and other changes that accompany the coordinated restoration of glomerular architecture after injury. |
| 160 | 1753704 | Endothelial and mesangial cells were positively identified from the early cultures (up to 10 days) with antibodies to a 350 kD protein, dipeptidyl peptidase IV, podocalyxin, factor VIII, OX-43 and with Bandeiraea simplicifolia (BS-I B4) lectin, and with antibodies to smooth muscle actin, desmin, Thy1.1 antigens and with Ricinus communis (RCA-1) lectin, respectively. |