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Gene Information
Gene symbol: CASP3
Gene name: caspase 3, apoptosis-related cysteine peptidase
HGNC ID: 1504
Synonyms: CPP32, CPP32B, Yama, apopain
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 35135431 | Immunohistochemical evaluation was performed using the following markers: cleaved caspase 3, inducible nitric oxide synthase, and tumor necrosis factor-alpha. |
| 2 | 35069207 | Podocytes injury is one of the leading causes of proteinuria in patients with diabetic nephropathy (DN), and is accompanied by podocytes apoptosis and the reduction of podocyte markers such as synaptopodin and nephrin. |
| 3 | 35069207 | The results show that administration of quercetin attenuated the level of podocyte apoptosis by decreasing the expression of pro-apoptotic protein Bax, cleaved caspase 3 and increasing the expression of anti-apoptotic protein Bcl-2 in the db/db mice and HG-induced MPs. |
| 4 | 35069207 | In vitro and vivo experiments confirmed that quercetin inhibited activation of the EGFR signaling pathway by decreasing phosphorylation of EGFR and ERK1/2. |
| 5 | 34938183 | AKT1, BCL2L1, CASP3, and MTOR were the core QRKSG targets in the treatment of NS. |
| 6 | 34938183 | AKT1, BCL2L1, CASP3, and MTOR were the core QRKSG targets in the treatment of NS. |
| 7 | 34938183 | AKT1, BCL2L1, CASP3, and MTOR were the core QRKSG targets in the treatment of NS. |
| 8 | 34938183 | Moreover, the expression levels of p-PI3K, p-AKT1, p-mTOR, and CASP3 in the QRKSG group significantly decreased, while BCL2L1 increased compared to the model group. |
| 9 | 34938183 | Moreover, the expression levels of p-PI3K, p-AKT1, p-mTOR, and CASP3 in the QRKSG group significantly decreased, while BCL2L1 increased compared to the model group. |
| 10 | 34938183 | Moreover, the expression levels of p-PI3K, p-AKT1, p-mTOR, and CASP3 in the QRKSG group significantly decreased, while BCL2L1 increased compared to the model group. |
| 11 | 34938183 | These findings established the underlying mechanism of QRKSG, such as promoting autophagy and anti-apoptosis through the expression of AKT1, CASP3, BCL2L1, and mTOR to protect podocytes and maintain renal tubular function. |
| 12 | 34938183 | These findings established the underlying mechanism of QRKSG, such as promoting autophagy and anti-apoptosis through the expression of AKT1, CASP3, BCL2L1, and mTOR to protect podocytes and maintain renal tubular function. |
| 13 | 34938183 | These findings established the underlying mechanism of QRKSG, such as promoting autophagy and anti-apoptosis through the expression of AKT1, CASP3, BCL2L1, and mTOR to protect podocytes and maintain renal tubular function. |
| 14 | 34867334 | Sanqi Oral Solution Mitigates Proteinuria in Rat Passive Heymann Nephritis and Blocks Podocyte Apoptosis via Nrf2/HO-1 Pathway. |
| 15 | 34867334 | Further studies showed that SQ treatment could significantly inhibit podocyte apoptosis in PHN rats and ADR-injured podocytes, and protein levels of Cleaved Caspase-3 or the ratio of Bax/Bcl-2 were significantly decreased with SQ treatment in vivo or in vitro. |
| 16 | 34867334 | Moreover, we found that the nuclear factor erythroid 2-related factor-2/heme oxygenase 1 (Nrf2/HO-1) pathway mediated the anti-apoptosis effective of SQ in podocyte. |
| 17 | 34867334 | Thus, SQ mitigates podocyte apoptosis and proteinuria in PHN rats via the Nrf2/HO-1 pathway. |
| 18 | 34856328 | Up-regulation of VSIG4 alleviates kidney transplantation-associated acute kidney injury through suppressing inflammation and ROS via regulation of AKT signaling. |
| 19 | 34856328 | We then found that exogenous VSIG4 markedly ameliorated histological changes in kidney of CI/KT mice by suppressing inflammation and apoptosis through restraining nuclear factor-κB (NF-κB) and Caspase-3 activation, respectively. |
| 20 | 34856328 | Oxidative stress and reactive oxygen species (ROS) accumulation in renal tissues were also mitigated by exogenous VSIG4 in CI/KT mice through improving nuclear factor-erythroid 2 related factor 2 (Nrf2) nuclear expression. |
| 21 | 34856328 | Mechanistically, VSIG4 directly interacted with AKT, and AKT activation was necessary for VSIG4 to govern all these above mentioned cellular processes. |
| 22 | 34856328 | Collectively, our findings demonstrated that VSIG4 could mitigate AKI in a CI/KT mouse model, and we identified VSIG4/AKT axis as a promising therapeutic target for the treatment of the disease. |
| 23 | 34700229 | Rapamycin attenuates PLA2R activation-mediated podocyte apoptosis via the PI3K/AKT/mTOR pathway. |
| 24 | 34700229 | Primary MN has been associated with circulating antibodies against native podocyte antigens, including phospholipase A2 receptor (PLA2R); however, precision therapy targeting the signaling cascade of PLA2R activation is lacking. |
| 25 | 34700229 | We demonstrated that podocyte apoptosis was induced by Group IB secretory phospholipase A2 (sPLA2IB) in a concentration- and time-dependent manner via upregulation of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mTOR, and inhibited by rapamycin or LY294002. |
| 26 | 34700229 | Furthermore, aberrant activation of the PI3K/AKT/mTOR pathway triggers both extrinsic (caspase-8 and caspase-3) and intrinsic (Bcl-2-associated X protein [BAX], B-cell lymphoma 2 [BCL-2], cytochrome c, caspase-9, and caspase-3) apoptotic cascades in podocytes. |
| 27 | 34700229 | The therapeutic implications of our findings are that strategies to reduce PLA2R activation and PI3K/AKT/mTOR pathway inhibition in PLA2R-activated podocytes help protect podocytes from apoptosis. |
| 28 | 34536756 | When compared to the MTX-treated rats, MTX+NG significantly reduced the levels of urea, creatinine, MDA, NO, TNFα, IL-6, and caspase-3 activity. |
| 29 | 34376476 | VDR/Atg3 Axis Regulates Slit Diaphragm to Tight Junction Transition via p62-Mediated Autophagy Pathway in Diabetic Nephropathy. |
| 30 | 34376476 | Here, we demonstrated that impaired autophagic flux blocked p62-mediated degradation of ZO-1 (TJ protein) and promoted podocytes injury via activation of caspase3 and caspase8. |
| 31 | 34376476 | In conclusion, our data provided the novel insight that VDR/Atg3 axis deficiency resulted in SD-TJ transition and foot processes effacement via blocking the p62-mediated autophagy pathway in DN. |
| 32 | 34095318 | After treatment with FK506, we measured 24-hour urinary albumin-to-creatinine ratios and creatinine clearance rates as well as major biochemical parameters such as glucose, insulin, serum creatinine, urea nitrogen, total cholesterol, triglycerides, alanine transaminase, and aspartate aminotransferase. |
| 33 | 34095318 | After treatment with FK506, we measured 24-hour urinary albumin-to-creatinine ratios and creatinine clearance rates as well as major biochemical parameters such as glucose, insulin, serum creatinine, urea nitrogen, total cholesterol, triglycerides, alanine transaminase, and aspartate aminotransferase. |
| 34 | 34095318 | Nephrin and TRPC6 protein expression and podocyte apoptotic rates in vivo and in vitro were measured using immunohistochemical staining, TUNEL assays, and flow cytometry, respectively. |
| 35 | 34095318 | Nephrin and TRPC6 protein expression and podocyte apoptotic rates in vivo and in vitro were measured using immunohistochemical staining, TUNEL assays, and flow cytometry, respectively. |
| 36 | 34095318 | Western blot was used to measure expression of cleaved-caspase-3 and bax/bcl-2. |
| 37 | 34095318 | Western blot was used to measure expression of cleaved-caspase-3 and bax/bcl-2. |
| 38 | 34095318 | Decreased expression of nephrin and increased expression of TRPC6, cleaved-caspase-3, and bax/bcl-2 ratios were found in podocytes, along with higher apoptotic percentage, while tacrolimus intervention counteracted the effect of HG on podocytes. |
| 39 | 34095318 | Decreased expression of nephrin and increased expression of TRPC6, cleaved-caspase-3, and bax/bcl-2 ratios were found in podocytes, along with higher apoptotic percentage, while tacrolimus intervention counteracted the effect of HG on podocytes. |
| 40 | 33776779 | Reduction in CHOP expression and IL-6 release was observed in jj primary aortic endothelial cells exposed to PA compared to Nj cells. |
| 41 | 33776779 | Upon Ang II treatment, primary podocytes from jj Gunn rats showed lower DNA fragmentation, cleaved caspase-3, and cleaved PARP induction than primary podocytes from Nj Gunn rats. |
| 42 | 33776779 | In HK2 cells, the induction by Ang II of HIF-1α and LOXl2 was significantly reduced by UCB pretreatment. |
| 43 | 33690262 | Gasdermin D Protects Mouse Podocytes Against High-Glucose-Induced Inflammation and Apoptosis via the C-Jun N-Terminal Kinase (JNK) Pathway. |
| 44 | 33690262 | We used western blot analysis, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and immunofluorescence to detect the expression and localization of GSDMD in high-glucose-induced podocytes, and the expression of apoptosis-related proteins Bax and Bcl-2, inflammatory factors IL-1ß, IL-6, and TNF-alpha, and JNK pathways in high-glucose-induced podocytes. |
| 45 | 33690262 | Western blot and immunofluorescence were used to detect the expression and localization of synaptopodin under GSDMD knockdown and JNK-specific blocker SP600125. |
| 46 | 33690262 | RESULTS We found that GSDMD knockdown and JNK inhibition reduced the expression of Bax, Bcl-2, cleaved caspase-3, IL-1ß, IL-6, and TNF-alpha. |
| 47 | 33675865 | Intermedin(IMD) is a novel member of the calcitonin/calcitonin gene-related peptide (CT/CGRP) family that has anti-inflammatory, antioxidant and anti-apoptosis properties. |
| 48 | 33675865 | IMD also improved the induction of slit diaphragm proteins, and restored the decreased Bcl-2 expression and suppressed Bax and caspase-3 induction in the diabetic glomeruli. |
| 49 | 33655586 | The expression of the inflammatory factors TNF-α, IL-1β, and IL-6 was determined by ELISA. |
| 50 | 33655586 | The expression of the inflammatory factors TNF-α, IL-1β, and IL-6 was determined by ELISA. |
| 51 | 33655586 | The expression of inflammatory proteins MCP-1, NLPR3, and ASC was detected by western blot. |
| 52 | 33655586 | The expression of inflammatory proteins MCP-1, NLPR3, and ASC was detected by western blot. |
| 53 | 33655586 | Apoptosis was detected by flow cytometry and apoptosis-related proteins Bcl-2, Bax, Caspase-3, 6, 9, and Cleaved caspase-3, 6, 9 were detected by western blot. |
| 54 | 33655586 | Apoptosis was detected by flow cytometry and apoptosis-related proteins Bcl-2, Bax, Caspase-3, 6, 9, and Cleaved caspase-3, 6, 9 were detected by western blot. |
| 55 | 33655586 | After high glucose induction, the expression of TNF-α, IL-1β, and IL-6 was increased and the expression of MCP-1, NLPR3, and ASC proteins was also increased (p < .001). |
| 56 | 33655586 | After high glucose induction, the expression of TNF-α, IL-1β, and IL-6 was increased and the expression of MCP-1, NLPR3, and ASC proteins was also increased (p < .001). |
| 57 | 33655586 | AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase-3, 6, 9, and promote the expression of Bcl-2 (p < .001). |
| 58 | 33655586 | AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase-3, 6, 9, and promote the expression of Bcl-2 (p < .001). |
| 59 | 33557007 | Therefore, MSC-treated animals exhibited lower levels of urinary albumin-to-creatinine ratio, less mesangial expansion, higher number of podocytes, up-regulation of mitochondria-related survival genes, a decrease in autophagy hyper-activation, and a potential decrease in cleaved-caspase 3 expression. |
| 60 | 33545631 | Podocyte RNF166 deficiency alleviates diabetic nephropathy by mitigating mitochondria impairment and apoptosis via regulation of CYLD signal. |
| 61 | 33545631 | RING-finger protein 166 (RNF166), composed of an N-terminal RING domain and C-terminal ubiquitin interaction motif, plays a critical role in mediating various cellular processes. |
| 62 | 33545631 | Furthermore, podocyte-specific RNF166 deficiency considerably mitigated apoptosis and mitochondrial impairments in glomeruli podocytes of STZ-challenged mice through suppressing Caspase-3 cleavage and improving mitochondrial fission-associated molecules. |
| 63 | 33545631 | Mechanistically, we demonstrated that RNF166 directly interacted with cylindromatosis (CYLD), and negatively regulated CYLD expression. |
| 64 | 33545631 | Notably, RNF166 knockout-attenuated mitochondrial damage and apoptosis were mainly through CYLD in podocytes upon HG stimulation. |
| 65 | 33545631 | Together, all these findings provided new insights into the novel effects of RNF166 on maintaining mitochondrial function and apoptosis in podocytes during DN progression both in vivo and in vitro through interacting with CYLD, indicating that RNF166/CYLD may be an innovative therapeutic target for developing effective strategy against DN development. |
| 66 | 33441223 | [Down-regulation of PHLPP1 expression ameliorates high glucose-induced autophagy inhibition and apoptosis promotion of podocytes by activating PI3K/AKT/mTOR pathway]. |
| 67 | 33441223 | [Down-regulation of PHLPP1 expression ameliorates high glucose-induced autophagy inhibition and apoptosis promotion of podocytes by activating PI3K/AKT/mTOR pathway]. |
| 68 | 33441223 | [Down-regulation of PHLPP1 expression ameliorates high glucose-induced autophagy inhibition and apoptosis promotion of podocytes by activating PI3K/AKT/mTOR pathway]. |
| 69 | 33441223 | Objective To investigate the expression of pleckstrin homology(PH) domain leucine-rich repeats protein phosphatase 1 (PHLPP1) in renal tissue of patients with diabetic nephropathy (DN) and its effect on podocyte autophagy and apoptosis, and to explore its related mechanism. |
| 70 | 33441223 | Objective To investigate the expression of pleckstrin homology(PH) domain leucine-rich repeats protein phosphatase 1 (PHLPP1) in renal tissue of patients with diabetic nephropathy (DN) and its effect on podocyte autophagy and apoptosis, and to explore its related mechanism. |
| 71 | 33441223 | Objective To investigate the expression of pleckstrin homology(PH) domain leucine-rich repeats protein phosphatase 1 (PHLPP1) in renal tissue of patients with diabetic nephropathy (DN) and its effect on podocyte autophagy and apoptosis, and to explore its related mechanism. |
| 72 | 33441223 | Methods Immunohistochemistry was used to detect PHLPP1 expression in renal tissue of patients with DN and non-diabetes, and immunofluorescence histochemical staining was used to detect the co-expression of nephrin and PHLPP1 to determine the localization of PHLPP1 in podocytes. |
| 73 | 33441223 | Methods Immunohistochemistry was used to detect PHLPP1 expression in renal tissue of patients with DN and non-diabetes, and immunofluorescence histochemical staining was used to detect the co-expression of nephrin and PHLPP1 to determine the localization of PHLPP1 in podocytes. |
| 74 | 33441223 | Methods Immunohistochemistry was used to detect PHLPP1 expression in renal tissue of patients with DN and non-diabetes, and immunofluorescence histochemical staining was used to detect the co-expression of nephrin and PHLPP1 to determine the localization of PHLPP1 in podocytes. |
| 75 | 33441223 | The formation of autophagic vesicles was observed by transmission electron microscope, and the protein expression levels of LC3, P62, PI3K, mTOR, p-mTOR, cleaved caspase 3 (c-caspase-3), AKT, p-AKT were detected by Western blotting. |
| 76 | 33441223 | The formation of autophagic vesicles was observed by transmission electron microscope, and the protein expression levels of LC3, P62, PI3K, mTOR, p-mTOR, cleaved caspase 3 (c-caspase-3), AKT, p-AKT were detected by Western blotting. |
| 77 | 33441223 | The formation of autophagic vesicles was observed by transmission electron microscope, and the protein expression levels of LC3, P62, PI3K, mTOR, p-mTOR, cleaved caspase 3 (c-caspase-3), AKT, p-AKT were detected by Western blotting. |
| 78 | 33441223 | Compared with NG group, the autophagy level of podocytes, the expression of PI3K and the phosphorylation level of mTOR in the HG group, HG combined with si-PHLPP1 group and HG combined with HCQ group were significantly reduced; the apoptosis rate and c-caspase-3 protein expression level were significantly enhanced; the phosphorylation level of AKT in the HG combined with si-PHLPP1 group significantly increased, but it in the other two groups significantly decreased. |
| 79 | 33441223 | Compared with NG group, the autophagy level of podocytes, the expression of PI3K and the phosphorylation level of mTOR in the HG group, HG combined with si-PHLPP1 group and HG combined with HCQ group were significantly reduced; the apoptosis rate and c-caspase-3 protein expression level were significantly enhanced; the phosphorylation level of AKT in the HG combined with si-PHLPP1 group significantly increased, but it in the other two groups significantly decreased. |
| 80 | 33441223 | Compared with NG group, the autophagy level of podocytes, the expression of PI3K and the phosphorylation level of mTOR in the HG group, HG combined with si-PHLPP1 group and HG combined with HCQ group were significantly reduced; the apoptosis rate and c-caspase-3 protein expression level were significantly enhanced; the phosphorylation level of AKT in the HG combined with si-PHLPP1 group significantly increased, but it in the other two groups significantly decreased. |
| 81 | 33441223 | Compared with HG group, the apoptosis rate and c-caspase-3 protein expression in the HG combined with si-PHLPP1 group were significantly reduced, while autophagy level, PI3K protein expression and phosphorylation level of mTOR and Akt protein were significantly elevated. |
| 82 | 33441223 | Compared with HG group, the apoptosis rate and c-caspase-3 protein expression in the HG combined with si-PHLPP1 group were significantly reduced, while autophagy level, PI3K protein expression and phosphorylation level of mTOR and Akt protein were significantly elevated. |
| 83 | 33441223 | Compared with HG group, the apoptosis rate and c-caspase-3 protein expression in the HG combined with si-PHLPP1 group were significantly reduced, while autophagy level, PI3K protein expression and phosphorylation level of mTOR and Akt protein were significantly elevated. |
| 84 | 33441223 | Conclusion PHLPP1 is highly expressed in renal tissue of patients with DN, and the down-regulated expression of PHLPP1 in podocytes can promote the autophagy of podocytes and reduced the apoptosis of podocytes by activating PI3K/AKT/mTOR pathway. |
| 85 | 33441223 | Conclusion PHLPP1 is highly expressed in renal tissue of patients with DN, and the down-regulated expression of PHLPP1 in podocytes can promote the autophagy of podocytes and reduced the apoptosis of podocytes by activating PI3K/AKT/mTOR pathway. |
| 86 | 33441223 | Conclusion PHLPP1 is highly expressed in renal tissue of patients with DN, and the down-regulated expression of PHLPP1 in podocytes can promote the autophagy of podocytes and reduced the apoptosis of podocytes by activating PI3K/AKT/mTOR pathway. |
| 87 | 33346797 | Upregulated LRRC55 and increased intracellular Ca2+ led to BK channel activation and the loss of intracellular potassium, resulting in apoptosome formation and caspase-3 activation in angiotensin II (Ang II)-treated podocytes. |
| 88 | 33346797 | Knockout of Lrrc55 or the BK channel prevented the BK current and ameliorated podocyte injury in Ang II-treated mice. |
| 89 | 33346797 | Upstream, NFATc3 regulated the expression of LRRC55. |
| 90 | 33323915 | RESULTS Paclitaxel restored downregulated expression of nephrin and synaptopodin and upregulated VEGF expression after injury induced by palmitate. |
| 91 | 33323915 | Four endoplasmic reticulum stress markers, ATF-6alpha, Bip, CHOP, and spliced xBP1, were significantly increased in palmitate-treated podocytes compared with control podocytes. |
| 92 | 33323915 | Paclitaxel alleviated the expression levels of the antioxidant molecules, Nrf-2, HO-1, SOD-1, and SOD-2. |
| 93 | 33323915 | The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3. |
| 94 | 33204708 | Curcumin Improves the Renal Autophagy in Rat Experimental Membranous Nephropathy via Regulating the PI3K/AKT/mTOR and Nrf2/HO-1 Signaling Pathways. |
| 95 | 33204708 | Western blot analyzed the levels of apoptosis, autophagy, PI3K/AKT/mTOR, and Nrf2/HO-1 pathway-associated proteins. |
| 96 | 33204708 | In addition, curcumin downregulated the expression of Bax, Caspase-3, p62, PI3K, p-AKT, and p-mTOR proteins and upregulated the Bcl-2, beclin1, LC3, Nrf2, and HO-1 levels in this animal model. |
| 97 | 33204708 | The results provide a scientific basis that curcumin could significantly alleviate the development of MN by inducing autophagy and alleviating renal oxidative stress through the PI3K/AKT/mTOR and Nrf2/HO-1 pathways. |
| 98 | 33147279 | In situ expression of Wilms Tumor 1 protein (WT1), light chain microtubule 1-associated protein (LC3) and caspase-3 protein were evaluated by immunohistochemistry. |
| 99 | 33147279 | In situ expression of Wilms Tumor 1 protein (WT1), light chain microtubule 1-associated protein (LC3) and caspase-3 protein were evaluated by immunohistochemistry. |
| 100 | 33147279 | Reduction in the density of WT1-labeled podocytes was observed for FSGS and MCD cases as compared to controls. |
| 101 | 33147279 | Reduction in the density of WT1-labeled podocytes was observed for FSGS and MCD cases as compared to controls. |
| 102 | 33147279 | The density of caspase-3-labeled podocytes in FSGS and MCD was higher than control group, and a higher number of podocytes with an evidence of necrosis was detected in FSGS cases than in MCD and control cases. |
| 103 | 33147279 | The density of caspase-3-labeled podocytes in FSGS and MCD was higher than control group, and a higher number of podocytes with an evidence of necrosis was detected in FSGS cases than in MCD and control cases. |
| 104 | 32931486 | The expression of IL-37, STAT3, and CypA was detected by RT-qPCR and western blot. |
| 105 | 32931486 | It inhibited the expression of the inflammation-related factors tumor necrosis factor alpha (TNF-alpha), IL-1ß, IL-6, malondialdehyde (MDA), and lactate dehydrogenase (LDH), and promoted the expression of superoxide dismutase (SOD) in high glucose-treated podocytes. |
| 106 | 32931486 | In addition, IL-37 inhibited the expression of the inflammation-related proteins MCP-1, NLRP3, ASC, and caspase-1. |
| 107 | 32931486 | IL-37 also inhibited high glucose-induced apoptosis of podocytes by inhibiting the expression of the apoptosis-related proteins Bax and cleaved caspase-3/6/9, and by promoting the expression of Bcl-2. |
| 108 | 32931486 | At the same time, we found that the STAT3/CypA signaling pathway was activated after induction by high glucose, while it was inhibited after treatment with IL-37. |
| 109 | 32931486 | Overexpression of STAT3 and CypA inhibited the effects of IL-37 on the alleviation of inflammation and oxidative stress and on the reduction of apoptosis of high glucose-treated podocytes. |
| 110 | 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. |
| 111 | 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. |
| 112 | 32786113 | Moreover AOPPs activated the accumulated FOXO3a by maintaining FOXO3a in the nucleus, and this process was dependent on ROS-mediated AKT signaling deactivation. |
| 113 | 32779844 | Tacrolimus ameliorates tubulointerstitial inflammation in diabetic nephropathy via inhibiting the NFATc1/TRPC6 pathway. |
| 114 | 32779844 | Macrophage infiltration and expression of IL-6, TNF-α, fibronectin, collagen 1 and cleaved caspase 3 were inhibited as well. |
| 115 | 32779844 | In addition, the expression of nuclear factor of activated T cell 1 (NFATc1) and transient receptor potential channel 6 (TRPC6) was up-regulated in the kidneys of DN patients and correlated with tubular injury and inflammation. |
| 116 | 32779844 | The expression of NFATc1 and TRPC6 also increased in the kidneys of db/db mice and HK-2 cells with high glucose (HG), while TAC inhibited these effects. |
| 117 | 32779844 | HG-induced inflammatory markers and apoptosis were reversed by TAC and NFATc1 siRNA in HK-2 cells, which was abolished by TRPC6 plasmid. |
| 118 | 32779844 | Furthermore, HG-induced TRPC6 expression was inhibited by NFATc1 siRNA, while NFATc1 nuclear translocation was inhibited by TAC, but was restored by TRPC6 plasmid in HK-2 cells under HG conditions. |
| 119 | 32779844 | These findings suggest that TAC ameliorates tubulointerstitial inflammation in DN through NFATc1/TRPC6 feedback loop. |
| 120 | 32765784 | Lycopene attenuates high glucose-mediated apoptosis in MPC5 podocytes by promoting autophagy via the PI3K/AKT signaling pathway. |
| 121 | 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. |
| 122 | 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. |
| 123 | 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. |
| 124 | 32765784 | In addition, under HG conditions, Lyc upregulated the phosphorylation levels of PI3K and AKT, and reduced HG- and LY-mediated MPC5 podocyte apoptosis. |
| 125 | 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. |
| 126 | 32696822 | MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy. |
| 127 | 32696822 | MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury. |
| 128 | 32696822 | Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear. |
| 129 | 32696822 | The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR. |
| 130 | 32696822 | The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay. |
| 131 | 32696822 | The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays. |
| 132 | 32696822 | The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay. |
| 133 | 32696822 | MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes. |
| 134 | 32696822 | MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes. |
| 135 | 32696822 | E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes. |
| 136 | 32696822 | MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes. |
| 137 | 32696822 | We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes. |
| 138 | 32696822 | These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression. |
| 139 | 32583562 | Smad3 signaling and transgelin expression are often activated during puromycin aminonucleoside (PAN)-induced podocyte injury. |
| 140 | 32583562 | The effects of SIS3 on the expression of the podocyte cytoskeletal proteins transgelin, p15INK4B , phosphor-smad3, phosphor-JAK/stat3, the apoptotic marker cleaved caspase 3, and c-myc were investigated using western blot. |
| 141 | 32583562 | Transgelin expression and Smad3 phosphorylation were increased in the MPC5 cell line with prolonged PAN treatment. |
| 142 | 32583562 | In addition, c-myc expression, p15INK4B , and JAK phosphorylation were all increased after treatment with PAN. |
| 143 | 32583562 | Moreover, stimulating podocytes directly with TGFβ-1 also led to enhanced expression of transgelin or phosphor-JAK/stat3, and this could be inhibited by SIS3. |
| 144 | 32583562 | In conclusion, transgelin expression was induced through the Smad3 signaling pathway during PAN-induced podocyte injury, and the resulting abnormal distribution of F-actin and the enhanced expression of transgelin could be reversed by blockade of this pathway. |
| 145 | 32537005 | In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65. |
| 146 | 32537005 | In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65. |
| 147 | 32537005 | In vitro, IL-17 induced podocyte apoptosis and reduced the expression of markers associated with podocytes, including Wilm's tumor 1, nephrin, synaptopodin and podocalyxin, whilst increasing the levels of Fas, Fas ligand (FasL), active-caspase-8, active-caspase-3 and phosphorylated-p65. |
| 148 | 32537005 | However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway. |
| 149 | 32537005 | However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway. |
| 150 | 32537005 | However, treatment with helenalin, a NF-κB inhibitor, decreased p65 phosphorylation, attenuated IL-17-induced podocyte apoptosis and suppressed the IL-17-activated Fas/FasL/caspase-8/caspase-3 apoptotic pathway. |
| 151 | 32537005 | Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner. |
| 152 | 32537005 | Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner. |
| 153 | 32537005 | Taken together, these observations suggest that IL-17 was highly expressed in renal tissues from patients with PNS, where it induced podocyte apoptosis by activating the Fas/FasL/caspase-8/caspase-3 apoptotic pathway in a NF-κB-dependent manner. |
| 154 | 32387304 | Perilipin2 overexpression reversed the effects of HG on inhibiting podocalyxin, nephrin, precursor (pro)-caspase-3/-9 and PPARγ protein expression and increasing cleaved caspase-3/-9 protein expression. |
| 155 | 32340263 | To estimate glomerular autophagy, immunohistochemistry for beclin-1 and LAMP-1 was performed. |
| 156 | 32340263 | LC3B and LAMP-1, autophagy markers, and caspase-3 and Bcl-2, apoptotic markers, were evaluated in renal cortex by western blot. |
| 157 | 32340263 | Vehicle-treated db/db mice had weak glomerular staining for beclin-1 and LAMP-1 and reduced Vv of autophagosomes, autolysosomes and lysosomes in podocytes. |
| 158 | 32340263 | Empagliflozin and linagliptin, both as monotherapy and in combination, enhanced the areas of glomerular staining for beclin-1 and LAMP-1 and increased Vv of autophagosomes and autolysosomes in podocytes. |
| 159 | 32256962 | The number of apoptotic cells was measured by the TUNEL assay, and apoptosis-related proteins BAX, caspase-3, and BCL-2 in the renal tissue were analyzed by western blot. |
| 160 | 32256962 | The number of apoptotic cells was measured by the TUNEL assay, and apoptosis-related proteins BAX, caspase-3, and BCL-2 in the renal tissue were analyzed by western blot. |
| 161 | 32256962 | The western blot results indicated that HSYA reversed the upregulation of BAX and caspase-3 and significantly increased BCL-2 in renal tissue. |
| 162 | 32256962 | The western blot results indicated that HSYA reversed the upregulation of BAX and caspase-3 and significantly increased BCL-2 in renal tissue. |
| 163 | 32119711 | This study aimed to investigate if and how ADP-ribosylation factor 6 (Arf6), a small GTP-binding protein, involves Ang II-induced cellular injury in cultured human podocytes. |
| 164 | 32119711 | Ang II significantly enhanced Arf6 expressions accompanied by increase of Arf6-GTP. |
| 165 | 32119711 | The TUNEL-positive cells as well as activated caspase 3, NADPH oxidase 4 protein (Nox4) and ROS levels were dramatically increased in Ang II-treated podocytes, which was prevented by secinH3, an Arf6 activity inhibitor. |
| 166 | 32119711 | Induction of ROS by Ang II was inhibited in podocytes with Nox4 knockdown. |
| 167 | 32119711 | Ang II-induced elevation of Nox4 and ROS was prevented by Arf6 knockdown. |
| 168 | 32119711 | Phpspho-Erk1/2Thr202/Tyr204 levels were upregulated remarkably following Ang II treatment, and Erk inhibitor LY3214996 significantly downregulated Nox4 expression. |
| 169 | 32119711 | Overexpression of CD2AP prevented Ang II-induced upregulation of Arf6-GTP. |
| 170 | 32119711 | We also provided evidence that Ang II activates Arf6 by degradation of CD2AP. |
| 171 | 32104249 | Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting. |
| 172 | 32104249 | Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting. |
| 173 | 32104249 | The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining. |
| 174 | 32104249 | The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining. |
| 175 | 32104249 | The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels. |
| 176 | 32104249 | The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels. |
| 177 | 32104249 | Notch1 was identified as a direct target of miR-145-5p. |
| 178 | 32104249 | Notch1 was identified as a direct target of miR-145-5p. |
| 179 | 32104249 | Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression. |
| 180 | 32104249 | Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression. |
| 181 | 32104249 | These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG. |
| 182 | 32104249 | These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG. |
| 183 | 32104249 | In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN. |
| 184 | 32104249 | In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN. |
| 185 | 32104249 | Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax. |
| 186 | 32104249 | Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax. |
| 187 | 32104249 | The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN. |
| 188 | 32104249 | The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN. |
| 189 | 31971826 | Aerobic Endurance Exercise Ameliorates Renal Vascular Sclerosis in Aged Mice by Regulating PI3K/AKT/mTOR Signaling Pathway. |
| 190 | 31971826 | In this study, we investigated the protective effect of aerobic endurance exercise on renal vascular sclerosis in aged mice and its effect on the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. |
| 191 | 31971826 | Furthermore, aerobic endurance exercise resulted in downregulation of Bax, Caspase 3, IL-6, and senescent cells and upregulation of Bcl-2. |
| 192 | 31971826 | The upregulation of PI3K and its downstream signal molecules AKT and mTOR after aerobic endurance exercise was further observed. |
| 193 | 31971826 | Our observations indicated that aerobic endurance exercise may inhibit renal vascular sclerosis in aged mice by regulating the PI3K/AKT/mTOR signaling pathway. |
| 194 | 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). |
| 195 | 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). |
| 196 | 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). |
| 197 | 31440817 | Increased expression of inflammation-associated gene sets and inflammatory Casps, including Casp12, was observed in these Casp3 KO kidneys. |
| 198 | 31371698 | Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1. |
| 199 | 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. |
| 200 | 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). |
| 201 | 31371698 | The podocyte damage and apoptosis due to PVT1 and FOXA1 were verified with in vivo experiments. |
| 202 | 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. |
| 203 | 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. |
| 204 | 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. |
| 205 | 31321239 | In elafibranor-treated HFD mice, increased insulin sensitivity, reduced obesity and body fat mass, decreased severity of steatohepatitis, increased renal expression of PPARα, PPARδ, SIRT1, and autophagy (Beclin-1 and LC3-II) as well as glomerular/renal tubular barrier markers [synaptopodin (podocyte marker), zona occludin-1, and cubulin], reduced renal oxidative stress and caspase-3, and less urinary 8-isoprostanes excretion were observed. |
| 206 | 31321239 | Acute incubation of podocytes and HK-2 cells with elafibranor or recombinant SIRT1 reversed the HFD-sera-induced oxidative stress, autophagy dysfunction, cell apoptosis, barrier marker loss, albumin endocytosis, and reuptake reduction. |
| 207 | 31321239 | Besides hepatoprotective and metabolic beneficial effects, current study showed that elafibranor inhibited the progression of HFD-induced CKD through activation of renal PPARα, PPARδ, SIRT1, autophagy, reduction of oxidative stress, and apoptosis in mice with steatohepatitis. |
| 208 | 31247189 | High glucose-induced apoptosis and necroptosis in podocytes is regulated by UCHL1 via RIPK1/RIPK3 pathway. |
| 209 | 31247189 | Recently, necroptosis has emerged as an important cell death model in many pathological conditions, which is regulated through RIPK1/RIPK3 pathway. |
| 210 | 31247189 | Herein, necroptosis and apoptosis were shown to be involved in podocyte injury induced by high glucose (HG), both in vitro and in vivo, with a high level of positive signaling markers RIPK1 (298.4 ± 17.35), cleaved caspase 3 (497.1 ± 23.09), RIPK3 (108.4 ± 14.92), and MLKL (470.4 ± 15.73) than the control groups. |
| 211 | 31247189 | Furthermore, UCHL1 was found to play a major role in promoting podocyte necroptosis by regulating the ubiquitination state of the RIPK1/RIPK3 pathway. |
| 212 | 31247189 | The half-life of RIPK1 and RIPK3 proteins reduced and the expression of RIPK1, RIPK3, and MLKL decreased significantly after the knockdown of UCHL1. |
| 213 | 31247189 | Thus, inhibiting UCHL1 to downregulate the RIPK1/RIPK3 pathway may be a novel strategy to protect the podocytes in DN patients. |
| 214 | 31025335 | miR-15b-5p ameliorated high glucose-induced podocyte injury through repressing apoptosis, oxidative stress, and inflammatory responses by targeting Sema3A. |
| 215 | 31025335 | Meanwhile, forced expression of miR-15b-5p apparently restrained HG-triggered apoptosis of podocytes, concomitant with downregulated in the proapoptotic protein markers Bax and cleavage caspase-3, and upregulated the antiapoptotic protein Bcl-2. |
| 216 | 31025335 | Simultaneously, introduction of miR-15b-5p repressed HG-induced oxidative stress damage in HG-treated podocytes, as evidenced by reduced MDA content, NOX4 expression, and enhanced activities of superoxide dismutase and catalase. |
| 217 | 31025335 | Moreover, enforced expression of miR-15b-5p remarkably restrained the HG-stimulated inflammatory response, as reflected by attenuated the level of the cytokines IL-1β, TNF-α, and IL-6. |
| 218 | 31025335 | More important, we also identified Sema3A as a direct target of miR-15b-5p. |
| 219 | 31025335 | Reverse transcription polymerase chain reaction and western blot subsequently confirmed that miR-15b-5p negatively modulated the level of Sema3A. |
| 220 | 31025335 | Mechanically, overexpression of Sema3A impeded the beneficial effects of miR-15b-5p on HG-mediated apoptosis, oxidative stress, and inflammatory response. |
| 221 | 31025335 | Altogether, these findings manifested that miR-15b-5p protectively antagonized HG-triggered podocyte damage through relieving HG-induced apoptosis, oxidative stress, and inflammatory process in podocytes by targeting Sema3A, suggesting that miR-15b-5p might be a new therapeutic agent to improve management of DN. |
| 222 | 31004300 | P2X7R, Bax, and Caspase-3 protein expression were detected by western blot and immunofluorescence analysis.The expression of P2X7R, ROS, Bax, and Caspase-3 in human podocytes incubated with oxLDL was significantly up-regulated and was found to have higher intracellular lipid accumulation and podocyte apoptosis compared with the NC group. |
| 223 | 31004300 | P2X7R, Bax, and Caspase-3 protein expression were detected by western blot and immunofluorescence analysis.The expression of P2X7R, ROS, Bax, and Caspase-3 in human podocytes incubated with oxLDL was significantly up-regulated and was found to have higher intracellular lipid accumulation and podocyte apoptosis compared with the NC group. |
| 224 | 31004300 | P2X7R, Bax, and Caspase-3 protein expression were detected by western blot and immunofluorescence analysis.The expression of P2X7R, ROS, Bax, and Caspase-3 in human podocytes incubated with oxLDL was significantly up-regulated and was found to have higher intracellular lipid accumulation and podocyte apoptosis compared with the NC group. |
| 225 | 31004300 | However, co-administration with A438079, ROS, Bax, and Caspase-3 expression both significantly down-regulate as well as lower lipid accumulation and cellular apoptosis in the oxLDL-induced podocyte group. |
| 226 | 31004300 | However, co-administration with A438079, ROS, Bax, and Caspase-3 expression both significantly down-regulate as well as lower lipid accumulation and cellular apoptosis in the oxLDL-induced podocyte group. |
| 227 | 31004300 | However, co-administration with A438079, ROS, Bax, and Caspase-3 expression both significantly down-regulate as well as lower lipid accumulation and cellular apoptosis in the oxLDL-induced podocyte group. |
| 228 | 31004300 | Additionally, we found that the anti-apoptotic effect of A438079 is correlated with ROS, Bax, and Caspase-3 expression down-regulated. |
| 229 | 31004300 | Additionally, we found that the anti-apoptotic effect of A438079 is correlated with ROS, Bax, and Caspase-3 expression down-regulated. |
| 230 | 31004300 | Additionally, we found that the anti-apoptotic effect of A438079 is correlated with ROS, Bax, and Caspase-3 expression down-regulated. |
| 231 | 30862678 | Dual specificity phosphatases (DUSPs) are a family of phosphatases mainly responsible for MAPK inhibition. |
| 232 | 30862678 | Diabetes-induced DUSP4 reduction enhanced p38 and c-Jun N-terminal kinase (JNK) activity and podocyte dysfunction. |
| 233 | 30862678 | The overexpression of DUSP4 prevented the activation of p38, JNK, caspase 3/7 activity, and NADPH oxidase 4 expression induced by high glucose level exposure. |
| 234 | 30862678 | These morphological changes were associated with profound podocyte foot process effacement, cell death, and sustained p38 and JNK activation. |
| 235 | 30862678 | Moreover, inhibition of protein kinase C-δ prevented DUSP4 expression decline and p38/JNK activation in the podocytes and renal cortex of diabetic mice. |
| 236 | 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). |
| 237 | 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). |
| 238 | 30805933 | A20 overexpression exerts protective effects on podocyte injury in lupus nephritis by downregulating UCH-L1. |
| 239 | 30805933 | The study aims to explore the effect of A20 on LN in relation to the nuclear factor-kappa B (NF-κB) signaling pathway. |
| 240 | 30805933 | Next, A20, UCH-L1, and NF-κB expression in LN patients and MRL/lpr mice was determined. |
| 241 | 30805933 | A20 was downregulated, whereas UCH-L1 was upregulated in LN. |
| 242 | 30805933 | Overexpressed A20 declined NF-κB, UCH-L1 expression, and the extent of p65 phosphorylation. |
| 243 | 30805933 | A20 overexpression or UCH-L1 inhibition increased expression of synaptoporin and nephrin but decreased desmin expression and ubiquitin accumulation level in podocytes. |
| 244 | 30805933 | Moreover, A20 overexpression or UCH-L1 inhibition increased the podocyte number but decreased protein level of cleaved caspase-3, podocyte lesion improvement, decreased foot process width, glomerulus basement membrane, and foot process fusion rate. |
| 245 | 30805933 | In addition, urine protein, blood urea nitrogen, serum creatinine, and ds-DNA antibody levels decreased with elevated A20 or depleted UCH-L1. |
| 246 | 30805933 | Collectively, it could be concluded that A20 protects against podocyte injury in LN via UCH-L1 by inactivating the NF-κB signaling pathway. |
| 247 | 30698047 | The apoptosis was further evidenced by increments of apoptosis regulator BAX (BAX) and caspase-3 expression. |
| 248 | 30698047 | The apoptosis was further evidenced by increments of apoptosis regulator BAX (BAX) and caspase-3 expression. |
| 249 | 30698047 | More importantly, overexpression of ERRα in MCs significantly triggered MC apoptosis in line with increased BAX and caspase-3 expression. |
| 250 | 30698047 | More importantly, overexpression of ERRα in MCs significantly triggered MC apoptosis in line with increased BAX and caspase-3 expression. |
| 251 | 30671964 | The objective of this study was to investigate the molecular mechanism of how TUG1 interferes with the expression of C/EBP homologous protein (CHOP), peroxisome-proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α), which contributes to the development of diabetic nephropathy. |
| 252 | 30671964 | The objective of this study was to investigate the molecular mechanism of how TUG1 interferes with the expression of C/EBP homologous protein (CHOP), peroxisome-proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α), which contributes to the development of diabetic nephropathy. |
| 253 | 30671964 | The objective of this study was to investigate the molecular mechanism of how TUG1 interferes with the expression of C/EBP homologous protein (CHOP), peroxisome-proliferator-activated receptor-γ coactivator-1 alpha (PGC-1α), which contributes to the development of diabetic nephropathy. |
| 254 | 30671964 | Real-time polymerase chain reaction and western blot analysis were performed to explore the regulatory relationship among TUG1, CHOP, PGC-1α, and caspase-3. |
| 255 | 30671964 | Real-time polymerase chain reaction and western blot analysis were performed to explore the regulatory relationship among TUG1, CHOP, PGC-1α, and caspase-3. |
| 256 | 30671964 | Real-time polymerase chain reaction and western blot analysis were performed to explore the regulatory relationship among TUG1, CHOP, PGC-1α, and caspase-3. |
| 257 | 30671964 | TUG1 was highly expressed in a cell following treatment with high glucose, and PGC-1α and cleaved caspase-3 levels were much lower, while CHOP level was much higher in high glucose group (HG), furthermore, CHOP inhibited PGC-1α expression. |
| 258 | 30671964 | TUG1 was highly expressed in a cell following treatment with high glucose, and PGC-1α and cleaved caspase-3 levels were much lower, while CHOP level was much higher in high glucose group (HG), furthermore, CHOP inhibited PGC-1α expression. |
| 259 | 30671964 | TUG1 was highly expressed in a cell following treatment with high glucose, and PGC-1α and cleaved caspase-3 levels were much lower, while CHOP level was much higher in high glucose group (HG), furthermore, CHOP inhibited PGC-1α expression. |
| 260 | 30671964 | TUG1 negatively regulated CHOP expression, and positively regulated PGC-1α expression. |
| 261 | 30671964 | TUG1 negatively regulated CHOP expression, and positively regulated PGC-1α expression. |
| 262 | 30671964 | TUG1 negatively regulated CHOP expression, and positively regulated PGC-1α expression. |
| 263 | 30671964 | Meanwhile, total caspase-3 level in cell treated with or without HG transfected with CHOP small interfering ribonucleic acid (siRNA), TUG1, and TUG1 siRNA showed no evident difference with their corresponding control, while CHOP siRNA and TUG1 evidently decreased, and TUG1 siRNA remarkably increased cleaved caspase-3 level in HG or normal glucose groups in comparison with corresponding control. |
| 264 | 30671964 | Meanwhile, total caspase-3 level in cell treated with or without HG transfected with CHOP small interfering ribonucleic acid (siRNA), TUG1, and TUG1 siRNA showed no evident difference with their corresponding control, while CHOP siRNA and TUG1 evidently decreased, and TUG1 siRNA remarkably increased cleaved caspase-3 level in HG or normal glucose groups in comparison with corresponding control. |
| 265 | 30671964 | Meanwhile, total caspase-3 level in cell treated with or without HG transfected with CHOP small interfering ribonucleic acid (siRNA), TUG1, and TUG1 siRNA showed no evident difference with their corresponding control, while CHOP siRNA and TUG1 evidently decreased, and TUG1 siRNA remarkably increased cleaved caspase-3 level in HG or normal glucose groups in comparison with corresponding control. |
| 266 | 30671964 | TUG1 and PGC-1α levels were much lower, while CHOP level was much higher in participants diagnosed with DN. |
| 267 | 30671964 | TUG1 and PGC-1α levels were much lower, while CHOP level was much higher in participants diagnosed with DN. |
| 268 | 30671964 | TUG1 and PGC-1α levels were much lower, while CHOP level was much higher in participants diagnosed with DN. |
| 269 | 30671964 | A higher level of CHOP protein and lower level of PGC-1α were observed in subjects diagnosed with DN. |
| 270 | 30671964 | A higher level of CHOP protein and lower level of PGC-1α were observed in subjects diagnosed with DN. |
| 271 | 30671964 | A higher level of CHOP protein and lower level of PGC-1α were observed in subjects diagnosed with DN. |
| 272 | 30548130 | The effect of hyperglycemia and angiotensin II on APJ was examined in cultured podocytes. |
| 273 | 30548130 | In podocytes stimulated with Pyr1 Apelin-13, a change in the phosphorylation status of the signaling proteins, AKT, ERK, and p70S6K, was observed with an increase 15 min after stimulation. |
| 274 | 30548130 | Apelin-13 decreased activity of Caspase-3 in podocytes after high glucose treatment reflecting an antiapoptotic effect of APJ stimulation. |
| 275 | 30548130 | In podocytes, APJ mRNA was downregulated in high glucose, when compared to normal glucose conditions and exposure to angiotensin II led to a further significant decrease in APJ mRNA. |
| 276 | 30548130 | Within the glomerulus, APJ is mainly localized in podocytes and in this cell type its activation by Apelin-13 abolishes the proapoptotic effect of high glucose, suggesting a potential therapeutic role of apelin and emerging agonists with extended half-life for therapy of DKD. |
| 277 | 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. |
| 278 | 30361091 | Down-regulation of IRAK1 attenuates podocyte apoptosis in diabetic nephropathy through PI3K/Akt signaling pathway. |
| 279 | 30361091 | Here, we found that Interleukin 1 receptor associated kinases (IRAK1) was up-regulated in kidney in both DN patients and high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice. |
| 280 | 30361091 | In vivo, down regulation of IRAK1 ameliorated renal injury and function, with lower podocyte apoptosis, increased expression of Nephrin, attenuated thickness of the glomerular basement membrane and podocyte footprocess effacement. |
| 281 | 30361091 | Furthermore, in vitro, down regulation of IRAK1 in podocytes treated with high glucose (HG), podocyte apoptosis and inflammatory cytokines were significantly decreased, but Nephrin increased. |
| 282 | 30361091 | Meanwhile, apoptosis-related genes caspase-3/-9 were inhibited and phosphorylation levels of PI3K/Akt were dramatically down regulated. |
| 283 | 30158674 | Podocyte-specific Bmp4-overexpressing mice displayed increased kidney BMP4 expression and mesangial matrix expansion but decreased nephrin expression and numbers of WT1-positive cells. |
| 284 | 30158674 | BMP4 decreased nephrin expression but increased cleaved caspase-3 levels. p38 suppression inhibited caspase-3 activation. |
| 285 | 30116378 | Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H2O2. |
| 286 | 30116378 | Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H2O2. |
| 287 | 30116378 | Furthermore, phosphorylation of the signaling molecules protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) 1/2 appeared to increase following HNK treatment. |
| 288 | 30116378 | Furthermore, phosphorylation of the signaling molecules protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) 1/2 appeared to increase following HNK treatment. |
| 289 | 30116378 | The anti-oxidative stress mechanisms of HNK are partly due to suppressing the expression of caspase-3 and caspase-9 and upregulating phosphorylated-Akt and -Erk 1/2. |
| 290 | 30116378 | The anti-oxidative stress mechanisms of HNK are partly due to suppressing the expression of caspase-3 and caspase-9 and upregulating phosphorylated-Akt and -Erk 1/2. |
| 291 | 29904949 | BMSCs could rescue injured podocytes from aberrant apoptosis and autophagy by regulating cleaved caspase-3, Bax, Bcl-2, LC3-II/I, and p62. |
| 292 | 29904949 | Suppression of the PI3 K/Akt/mTOR signaling pathway is likely one of the main mechanisms underlying the protective action of BMSCs transfected with miR-124a. |
| 293 | 29860655 | Cisplatin increased serum urea and serum creatinine levels and caused an increase in tubular necrosis scores (TNS), HPS, NF-κB/p65, 8-OHdG, and caspase-3 expressions (p < 0.05). |
| 294 | 29860655 | Cisplatin increased serum urea and serum creatinine levels and caused an increase in tubular necrosis scores (TNS), HPS, NF-κB/p65, 8-OHdG, and caspase-3 expressions (p < 0.05). |
| 295 | 29860655 | Amifostine, curcumin, and melatonin reduced the increases in serum urea and serum creatinine levels following cisplatin administration and reduced the levels of TNS, HPS, NF-κB/p65, 8-OHdG, and caspase-3 expressions (p < 0.05). |
| 296 | 29860655 | Amifostine, curcumin, and melatonin reduced the increases in serum urea and serum creatinine levels following cisplatin administration and reduced the levels of TNS, HPS, NF-κB/p65, 8-OHdG, and caspase-3 expressions (p < 0.05). |
| 297 | 29843457 | TAU limited proteinuria and podocytes foot processes effacement, and balanced slit diaphragm nephrin and glomerular claudin 1 expressions. |
| 298 | 29843457 | Remarkably, TAU downregulated glomerular ER stress markers (GRP78, GRP94), pro-apoptotic C/EBP homologous protein, activated caspase 3, tubular caspase1, and mitochondrial chaperone GRP75, but maintained anti-apoptotic HSP25. |
| 299 | 29746568 | The protective effect of the EP2 receptor on TGF-β1 induced podocyte injury via the PI3K / Akt signaling pathway. |
| 300 | 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. |
| 301 | 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. |
| 302 | 29746568 | This causes the interaction of nephrin, podocin and CD2AP resulting the inhibition of apoptosis induced by activation of the PI3K / Akt signaling pathway. |
| 303 | 29724888 | After exposing cells to TNF-α, we determined the expression levels of heterogeneous nuclear ribonucleoprotein K (hnRNP K) and cellular FLICE-inhibitory protein (c-FLIP) and the phosphorylation levels of glycogen synthase kinase β (GSK3β) and extracellular signal-regulated kinase (ERK). |
| 304 | 29724888 | After exposing cells to TNF-α, we determined the expression levels of heterogeneous nuclear ribonucleoprotein K (hnRNP K) and cellular FLICE-inhibitory protein (c-FLIP) and the phosphorylation levels of glycogen synthase kinase β (GSK3β) and extracellular signal-regulated kinase (ERK). |
| 305 | 29724888 | We then knocked down or overexpressed the levels of hnRNP K and observed its effects on the expressions of c-FLIP, caspase-8, caspase-3, and the phosphorylation of GSK3β and ERK. |
| 306 | 29724888 | We then knocked down or overexpressed the levels of hnRNP K and observed its effects on the expressions of c-FLIP, caspase-8, caspase-3, and the phosphorylation of GSK3β and ERK. |
| 307 | 29724888 | We found that TNF-α induced apoptosis in podocytes and that the expressions of hnRNP K and c-FLIP were significantly decreased, whereas the phosphorylations of GSK3β and ERK were significantly increased. |
| 308 | 29724888 | We found that TNF-α induced apoptosis in podocytes and that the expressions of hnRNP K and c-FLIP were significantly decreased, whereas the phosphorylations of GSK3β and ERK were significantly increased. |
| 309 | 29724888 | Both gene knockdown and overexpression of hnRPN K resulted in varied expressions/phosphorylations of c-FLIP, GSK3β, and ERK. |
| 310 | 29724888 | Both gene knockdown and overexpression of hnRPN K resulted in varied expressions/phosphorylations of c-FLIP, GSK3β, and ERK. |
| 311 | 29724888 | In conclusion, down-regulated expression of hnRNP K by TNF-α resulted in a decrease in the expression of c-FLIP as well as increases in phosphorylated GSK3β, ERK, caspase-8, and caspase-3, and then critically contributed to the podocyte apoptosis. |
| 312 | 29724888 | In conclusion, down-regulated expression of hnRNP K by TNF-α resulted in a decrease in the expression of c-FLIP as well as increases in phosphorylated GSK3β, ERK, caspase-8, and caspase-3, and then critically contributed to the podocyte apoptosis. |
| 313 | 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. |
| 314 | 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. |
| 315 | 29572435 | Wnt/b-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by β-arrestin 1/2 overexpression and high glucose. |
| 316 | 29367812 | We noted a reduction of insulin-like growth factor 1 receptor (IGFR1) expression, decrease in extracellular signal-regulated kinase (ERK) activation, decrease in reactive oxygen species (ROS), and decrease in cleaved-caspase 3 expression. |
| 317 | 29367812 | We found an increase in [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) and an increase in matrix metalloproteinases (MMP-2 and MMP-9) activity. |
| 318 | 29367812 | In isolated podocytes, we confirmed reduction of ERα expression in conjunction with a decrease in IGFR1 expression, ERK and increase of MMP-2 similar to that of our in vitro treatment with RSV. |
| 319 | 29315280 | This study aimed to investigate the underlying mechanisms by which gremlin mediates the pathogenesis of DN via transforming growth factor-β (TGF-β) signaling pathways. |
| 320 | 29315280 | The gremlin overexpression significantly suppressed the expression of nephrin and synaptopodin. |
| 321 | 29315280 | The phosphorylation of canonical TGF-b signaling pathway components, including Smad2/3 and MKK, was increased in the gremlin-overexpressing group. |
| 322 | 29315280 | In addition, the expression levels of Bax and cleaved caspase-3 were also higher in the gremlin-overexpressing group. |
| 323 | 29312514 | TRPC6 plays a critical role in proteinuric kidney diseases, and TRPC3 is involved in tubulointerstitial damage and renal fibrosis in obstructed kidneys. |
| 324 | 29312514 | In addition, we observed decreased expression of anti-apoptotic Bcl2 and increased expression of pro-apoptotic cleaved caspase 3 in WT diabetic mice, but such changes were not significant in TRPC3/6/7-/- diabetic mice. |
| 325 | 29312514 | Western blot and immunohistochemistry revealed that TGFβ1, p-Smad2/3, and fibronectin were upregulated in WT diabetic mice; however, expression of these signaling molecules was not changed in TRPC3/6/7-/- diabetic mice. |
| 326 | 29245956 | Protein expressions of inflammatory (MMP-9/TNF-α/NF-κB/IL-1ß/ICAM-1), oxidative-stress (NOX-1/NOX-2/oxidized protein), apoptotic (mitochondrial-Bax/cleaved-caspase-3/cleaved-PARP) and fibrotic/DNA-damaged (Smad3/TGF-ß/γ-H2AX) biomarkers showed an identical pattern, whereas anti-fibrotic (BMP-2/Smad1/5), anti-apoptotic/endothelial-integrity (Bcl-2/eNOS) and podocyte-integrity (ZO-1/p-cadherin) biomarkers exhibited an opposite pattern of kidney-injury score among the six groups (all P>0.0001). |
| 327 | 29245956 | Cellular expressions of inflammatory (CD14/CD68) and glomerulus/tubular-injury (WT-1/KIM-1) biomarkers displayed an identical pattern, whereas glomerulus/podocyte-component (dystroglycan/nephrin/ZO-1/fibronectin/p-cadherin) biomarkers showed an opposite kidney-injury score among the six groups (all P<0.0001). |
| 328 | 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). |
| 329 | 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. |
| 330 | 29110957 | The kidney expresses protease-activated receptor-1 (PAR-1). |
| 331 | 29110957 | PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood. |
| 332 | 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. |
| 333 | 29110957 | In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes. |
| 334 | 28972886 | PF increased expression of synaptopodin and decreased expression of desmin, demonstrating a protective effect in podocyte injury. |
| 335 | 28972886 | Further studies revealed that PF upregulated Peroxisome proliferator-activated receptor gamma (PPARγ) and restrained Angiopointin-like 4 (ANGPTL4) in kidney tissue. |
| 336 | 28972886 | In vitro study, PF reduced Caspase3 and Bax and increased Bcl-2, indicating that the apoptosis rate of podocytes induced by ADR was reduced by PF. |
| 337 | 28849106 | Advanced glycation end products induce the apoptosis of and inflammation in mouse podocytes through CXCL9-mediated JAK2/STAT3 pathway activation. |
| 338 | 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). |
| 339 | 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. |
| 340 | 28849106 | The knockdown of CXCL9 also led to the inactivation of the Janus kinase 2 (JAK2)/STAT3 pathway. |
| 341 | 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. |
| 342 | 31966749 | Western blots were carried out for the related protein expression in podocytes, including CXCR3, Nephrin, Podocin, Bcl-2, Bax, and Caspase-3. |
| 343 | 31966749 | Western blots were carried out for the related protein expression in podocytes, including CXCR3, Nephrin, Podocin, Bcl-2, Bax, and Caspase-3. |
| 344 | 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. |
| 345 | 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. |
| 346 | 28722118 | In vivo and in vitro studies demonstrated that loss of AT2 R was associated with elevated NADPH oxidase 4 levels, which in turn stimulated ectopic hedgehog interacting protein (Hhip) gene expression in podocytes. |
| 347 | 28722118 | Consequently, ectopic Hhip expression activation either triggers caspase-3 and p53-related apoptotic processes resulting in podocyte loss, or activates TGFβ1-Smad2/3 cascades and α-SMA expression to transform differentiated podocytes to undifferentiated podocyte-derived fibrotic cells. |
| 348 | 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. |
| 349 | 28642201 | The molecular mechanism was associated with the upregulation of Bcl-2 and the downregulation of Bax. |
| 350 | 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). |
| 351 | 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). |
| 352 | 28392397 | TMEM16A exacerbates renal injury by activating P38/JNK signaling pathway to promote podocyte apoptosis in diabetic nephropathy mice. |
| 353 | 28392397 | Moreover, reverse transcription-polymerase chain reaction (RT-PCR) amplification, Western blot detection, Periodic Acid Schiff (PAS) staining and immunohistochemical analysis confirmed that TMEM16A deficiency alleviated renal injury in diabetic mice and TMEM16A knockout diabetic mice were protected from the HFD-induced reduction in Nephrin expression. |
| 354 | 28392397 | RT-PCR and Western blot exhibited that apoptosis-related genes including apoptosis-inducing factor (AIF) and cystinylaspartate specific protease-3/-9 (caspase-3/-9) were dramatically down regulated in siRNA-TMEM16A group, compared with Model group. |
| 355 | 28392397 | Phosphorylation levels of P38 and JNK in siRNA-TMEM16A group were lower than that of the Model group. |
| 356 | 28337255 | The kidney protein expressions of inflammation (TNF-α/NF-κB/MMP-9/iNOS/RANTES), oxidative stress (NOX-1/NOX-2/NOX-4/oxidized protein), apoptosis (cleaved caspase-3/cleaved PARP/Bax), DNA-damaged marker (γ-H2AX) and fibrosis (p-mad3/TFG-β) showed identical patterns of creatinine level, whereas kidney protein expressions of GLP-1R showed a progressive increase from SC to CRS-Mel-Ex4 (all P<0.0001). |
| 357 | 28337255 | Cellular expressions of inflammatory (CD14/CD68), DNA/kidney-damaged (γ-H2AX/KIM-1) and podocyte/renal tubule dysfunction signaling (β-catenin/Wnt1/Wnt4) biomarkers in kidney tissue exhibited an identical pattern of creatinine level (all P<0.0001). |
| 358 | 27882943 | Here we show that the expression levels of Mtdh and phosphorylated p38 mitogen-activated protein kinase (MAPK) are significantly increased, whereas those of the microRNA-30 family members (miR-30s) are considerably reduced in the glomeruli of DN rat model and in high glucose (HG)-induced conditionally immortalized mouse podocytes (MPC5). |
| 359 | 27882943 | The inhibition of Mtdh expression, using small interfering RNA, but not Mtdh overexpression, was shown to inhibit HG-induced MPC5 apoptosis and p38 MAPK pathway, and Bax and cleaved caspase 3 expression. |
| 360 | 27882943 | This was shown to be similar to the effects of p38 MAPK inhibitor (SB203580). |
| 361 | 27882943 | Our results demonstrate that Mtdh is a potent modulator of podocyte apoptosis, and that it represents the target of miR-30 miRNAs, facilitating podocyte apoptosis through the activation of HG-induced p38 MAPK-dependent pathway. |
| 362 | 27836988 | Treatment with RTX before radiation exposure partially protected podocytes from SMPDL3b loss, cytoskeletal remodeling, and caspase 3 cleavage. |
| 363 | 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. |
| 364 | 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. |
| 365 | 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. |
| 366 | 27580845 | Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signaling, thereby protecting podocytes from PAN-induced injury. |
| 367 | 27479491 | Knockdown of Expression of Cdk5 or p35 (a Cdk5 Activator) Results in Podocyte Apoptosis. |
| 368 | 27479491 | Knockdown of Expression of Cdk5 or p35 (a Cdk5 Activator) Results in Podocyte Apoptosis. |
| 369 | 27479491 | Knockdown of Expression of Cdk5 or p35 (a Cdk5 Activator) Results in Podocyte Apoptosis. |
| 370 | 27479491 | Cdk5 is a cyclin-dependent protein kinase which is predominantly regulated by p35. |
| 371 | 27479491 | Cdk5 is a cyclin-dependent protein kinase which is predominantly regulated by p35. |
| 372 | 27479491 | Cdk5 is a cyclin-dependent protein kinase which is predominantly regulated by p35. |
| 373 | 27479491 | To study the role of Cdk5/p35 in podocyte survival, we first applied western blotting (WB) analysis to confirm the time-course expression of Cdk5 and p35 during kidney development and in cultured immortalized mouse podocytes. |
| 374 | 27479491 | To study the role of Cdk5/p35 in podocyte survival, we first applied western blotting (WB) analysis to confirm the time-course expression of Cdk5 and p35 during kidney development and in cultured immortalized mouse podocytes. |
| 375 | 27479491 | To study the role of Cdk5/p35 in podocyte survival, we first applied western blotting (WB) analysis to confirm the time-course expression of Cdk5 and p35 during kidney development and in cultured immortalized mouse podocytes. |
| 376 | 27479491 | To deregulate the expression of Cdk5 or p35 in mouse podocytes, we used RNAi and analyzed cell function and apoptosis assaying for podocyte specific marker Wilms Tumor 1 (WT1) and cleaved caspase 3, respectively. |
| 377 | 27479491 | To deregulate the expression of Cdk5 or p35 in mouse podocytes, we used RNAi and analyzed cell function and apoptosis assaying for podocyte specific marker Wilms Tumor 1 (WT1) and cleaved caspase 3, respectively. |
| 378 | 27479491 | To deregulate the expression of Cdk5 or p35 in mouse podocytes, we used RNAi and analyzed cell function and apoptosis assaying for podocyte specific marker Wilms Tumor 1 (WT1) and cleaved caspase 3, respectively. |
| 379 | 27479491 | We found that depletion of Cdk5 causes decreased expression of WT1 and apoptosis. |
| 380 | 27479491 | We found that depletion of Cdk5 causes decreased expression of WT1 and apoptosis. |
| 381 | 27479491 | We found that depletion of Cdk5 causes decreased expression of WT1 and apoptosis. |
| 382 | 27479491 | It is noteworthy, however, that downregulation of p35 reduced Cdk5 activity, but had no effect on cleaved caspase 3 expression. |
| 383 | 27479491 | It is noteworthy, however, that downregulation of p35 reduced Cdk5 activity, but had no effect on cleaved caspase 3 expression. |
| 384 | 27479491 | It is noteworthy, however, that downregulation of p35 reduced Cdk5 activity, but had no effect on cleaved caspase 3 expression. |
| 385 | 27479491 | On the other hand increased apoptosis could be detected in p35-deregulated podocytes using the TUNEL analysis and immunofluorescent staining with cleaved caspase3 antibody. |
| 386 | 27479491 | On the other hand increased apoptosis could be detected in p35-deregulated podocytes using the TUNEL analysis and immunofluorescent staining with cleaved caspase3 antibody. |
| 387 | 27479491 | On the other hand increased apoptosis could be detected in p35-deregulated podocytes using the TUNEL analysis and immunofluorescent staining with cleaved caspase3 antibody. |
| 388 | 27479491 | Viability of podocytes was decreased in both Cdk5 and p35 knockdown cells. |
| 389 | 27479491 | Viability of podocytes was decreased in both Cdk5 and p35 knockdown cells. |
| 390 | 27479491 | Viability of podocytes was decreased in both Cdk5 and p35 knockdown cells. |
| 391 | 27479491 | Knocking down Cdk5 or p35 gene by RNAi does not affect the cycline I expression, another Cdk5 activator in podocyes. |
| 392 | 27479491 | Knocking down Cdk5 or p35 gene by RNAi does not affect the cycline I expression, another Cdk5 activator in podocyes. |
| 393 | 27479491 | Knocking down Cdk5 or p35 gene by RNAi does not affect the cycline I expression, another Cdk5 activator in podocyes. |
| 394 | 27479491 | We conclude that Cdk5 and p35 play a crucial role in maintaining podocyte differentiation and survival, and suggest these proteins as targets for therapeutic intervention in podocyte-damaged kidney diseases. |
| 395 | 27479491 | We conclude that Cdk5 and p35 play a crucial role in maintaining podocyte differentiation and survival, and suggest these proteins as targets for therapeutic intervention in podocyte-damaged kidney diseases. |
| 396 | 27479491 | We conclude that Cdk5 and p35 play a crucial role in maintaining podocyte differentiation and survival, and suggest these proteins as targets for therapeutic intervention in podocyte-damaged kidney diseases. |
| 397 | 27226110 | Specific endothelial heparin-binding EGF-like growth factor deletion ameliorates renal injury induced by chronic angiotensin II infusion. |
| 398 | 27226110 | Transactivation of EGF receptor (EGFR) by angiotensin II (Ang II) plays important roles in the initiation and progression of chronic kidney diseases. |
| 399 | 27226110 | Studies suggest that heparin-binding EGF-like factor (HB-EGF) may be a critical mediator in this process, but its role in vivo has not been investigated. |
| 400 | 27226110 | In the current study, we found that in response to Ang II infusion, kidneys from endothelial HB-EGF deletion mice had significantly reduced EGFR activation compared with controls. |
| 401 | 27226110 | Meanwhile, deletion of endothelial HB-EGF expression decreased Ang II infusion related renal injury, as demonstrated by 1) less albuminuria; 2) less glomerulosclerosis; 3) preserved endothelial integrity and decreased podocyte injury, as shown by greater glomerular tuft area and WT1-positive cells, and fewer apoptotic cells measured by cleaved caspase 3 staining; 4) reduced inflammation in the perivascular area and interstitium measured by F4/80 and CD3 immunostaining; and 5) reduced renal fibrosis. |
| 402 | 27226110 | In conclusion, our results suggest that shedding of HB-EGF from endothelium plays an important role in Ang II-induced renal injury by linking Ang II-AT1R with EGFR transactivation. |
| 403 | 27220903 | Western blot analysis was performed to detect the expression of Nephrin, B cell lymphoma‑2 (Bcl‑2)‑associated X protein (Bax), Bcl-2, Caspase-3, Janus kinase (JAK)2 and Signal transducer and activator of transcription (STAT)3 in podocytes. |
| 404 | 27037275 | The protein expressions of inflammatory (toll-like receptor 4, inducible nitric oxide synthase, interleukin-1β), apoptotic (mitochondrial Bax, cleaved caspase-3 and poly(ADP-ribose) polymerase, p53), podocyte integrity (E-cadherin, P-cadherin), and cell survival (phosphatidylinositol-3-kinase/AKT/mammalian target of rapamycin) biomarkers, as well the podocyte dysfunction biomarkers (Wnt1/Wnt4/β-catenin) displayed a pattern identical to that of creatinine level among the five groups (all p < 0.001). |
| 405 | 27037275 | Microscopic findings demonstrated that podocyte dysfunction (Wnt1/Wnt4/β-catenin expression) and inflammatory (CD14 and F4/80-positively stained cells) biomarkers exhibited an identical pattern, whereas that of antioxidant (HO-1(+), NQO-1(+) cells) biomarkers showed an opposite pattern compared to that of creatinine level among the five groups (all p < 0.001). |
| 406 | 26999661 | These beneficial effects of UDCA or 4-PBA on DN were associated with the inhibition of ER stress, as evidenced by the decreased expression of BiP, phospho-IRE1α, phospho-eIF2α, CHOP, ATF-6 and spliced X-box binding protein-1 in vitro and in vivo. |
| 407 | 26999661 | UDCA or 4-PBA prevented hyperglycemia-induced or high glucose (HG)-induced apoptosis in podocytes in vivo and in vitro via the inhibition of caspase-3 and caspase-12 activation. |
| 408 | 26953552 | Ubiquitin-specific protease 22 (USP22) has been reported to mediate various cellular processes, including cell proliferation and apoptosis. |
| 409 | 26953552 | Silencing of USP22 in podocytes attenuated high d-glucose-induced apoptosis and inflammatory responses, evidenced by increases in proliferation and MMP levels and decreases in the apoptotic rate, ROS production, the Bax/Bcl-2 ratio, caspase-3 expression and secretion of TNF-α, IL-1β, IL-6 and TGF-β1. |
| 410 | 26953552 | Similar to the protective effect of USP22 knockdown, resveratrol (RSV) depressed not only high d-glucose- and USP22 overexpression-induced cytotoxicity, but also the secretion of TNF-α, IL-1β, IL-6 and TGF-β1. |
| 411 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 412 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 413 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 414 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 415 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 416 | 26832955 | Caspase-1, but Not Caspase-3, Promotes Diabetic Nephropathy. |
| 417 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 418 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 419 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 420 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 421 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 422 | 26832955 | Here, we administered two partially disjunct polycaspase inhibitors in 8-week-old diabetic (db/db) mice: M-920 (inhibiting caspase-1, -3, -4, -5, -6, -7, and -8) and CIX (inhibiting caspase-3, -6, -7, -8, and -10). |
| 423 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 424 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 425 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 426 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 427 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 428 | 26832955 | Accordingly, analysis of gene expression data in the Nephromine database revealed persistently elevated glomerular expression of inflammasome markers (NLRP3, CASP1, PYCARD, IL-18, IL-1β), but not of apoptosis markers (CASP3, CASP7, PARP1), in patients with and murine models of dNP. |
| 429 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 430 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 431 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 432 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 433 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 434 | 26832955 | In vitro, increased levels of markers of inflammasome activation (Nlrp3, caspase-1 cleavage) preceded those of markers of apoptosis activation (caspase-3 and -7, PARP1 cleavage) in glucose-stressed podocytes. |
| 435 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 436 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 437 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 438 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 439 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 440 | 26832955 | Finally, caspase-3 deficiency did not protect mice from dNP, whereas both homozygous and hemizygous caspase-1 deficiency did. |
| 441 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 442 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 443 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 444 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 445 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 446 | 26832955 | Hence, these results suggest caspase-3-dependent cell death has a negligible effect, whereas caspase-1-dependent inflammasome activation has a crucial function in the establishment of dNP. |
| 447 | 26667396 | The renoprotective effects of Flos A. manihot are related to inhibition of caspase-3 and caspase-8 overexpression, reduction of the infiltration of ED1(+) and ED3(+) macrophages, downregulation of oxidative stress, inhibition of the p38 mitogen-activated protein kinase and serine/threonine kinase pathways and suppression of transforming growth factor-β1 and tumour necrosis factor-α expression. |
| 448 | 26315992 | In AFB1-treated group, focal tubulo-interstitial affection in the form of tubular cytoplasmic vacuolation, mitochondrial disruption, numerous lysosomes, marked increase in collagen deposition and in caspase-3 expression were observed. |
| 449 | 26191142 | The direct interaction between miR-34c and the 3'-untranslated region (UTR) of Notch1 and Jagged1 was validated by dual-luciferase reporter assay. |
| 450 | 26191142 | Moreover, Notch1 and Jagged1 as putative targets of miR-34c were downregulated by miR-34c overexpression in HG-treated podocytes. |
| 451 | 26191142 | Overexpression of miR-34c inhibited HG-induced Notch signaling pathway activation, as indicated by decreased expression of the Notch intracellular domain (NICD) and downstream genes including Hes1 and Hey1. |
| 452 | 26191142 | Furthermore, miR-34c overexpression increased the expression of the anti-apoptotic gene Bcl-2, and decreased the expression of the pro-apoptotic protein Bax and cleaved Caspase-3. |
| 453 | 26191142 | Additionally, the phosphorylation of p53 was also downregulated by miR-34c overexpression. |
| 454 | 26191142 | Taken together, our findings suggest that miR-34c overexpression inhibits the Notch signaling pathway by targeting Notch1 and Jaggged1 in HG-treated podocytes, representing a novel and potential therapeutic target for the treatment of diabetic nephropathy. |
| 455 | 25953318 | We observed significant increases in the protein expression of p27, p21, phospho-eukaryotic elongation factor 4E-binding protein 1, and phospho-p70 S6 ribosomal protein kinase, in both cultured podocytes exposed to high-glucose (HG) medium, and streptozotocin-induced diabetes mellitus (DM) rat glomeruli. |
| 456 | 25953318 | Increased protein expression of cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase, together with increased Bax/Bcl-2 ratios, were also observed in HG-stimulated podocytes and DM glomeruli. |
| 457 | 25808596 | A human podocyte cell line was used as a model to examine the regulation of the expression of AT1R, PRR, TNF-α and CTGF by IgA-HMC media. |
| 458 | 25808596 | Podocytic nephrin expression, annexin V binding and caspase 3 activity were used as the functional readout of podocytic apoptosis. |
| 459 | 25808596 | IgA-HMC media significantly up-regulated the expression of AT1R and PRR, down-regulated nephrin expression and induced apoptosis in podocytes. |
| 460 | 25808596 | Mono-blockade of AT1R, PRR, TNF-α or CTGF partially reduced podocytic apoptosis. |
| 461 | 25808596 | IgA-HMC media activated NFκB, notch1 and HEY1 expression by podocytes and dual blockade of AT1R with PRR, or anti-TNF-α with anti-CTGF, effectively rescued the podocytic apoptosis induced by IgA-HMC media. |
| 462 | 25808596 | Our data suggests that pIgA-activated HMC up-regulates the expression of AT1R and PRR expression by podocytes and the associated activation of NFκB and notch signalling pathways play an essential role in the podocytic apoptosis induced by glomerulo-podocytic communication in IgAN. |
| 463 | 25808596 | Simultaneously targeting the AT1R and PRR could be a potential therapeutic option to reduce the podocytic injury in IgAN. |
| 464 | 25736496 | These isolated Nestin(+) cells expressed the typical cell-surface marker of MSC, including Sca-1, CD44, CD106, NG2 and PDGFR-α. |
| 465 | 25715637 | Double immunofluorescence analysis shows the precise distribution of TLR2 by showing the colocalization of TLR2 in glomeruli with synaptopodin, a podocyte marker, and Tie2, an endothelial marker. |
| 466 | 25715637 | Double immunofluorescence analysis shows the precise distribution of TLR2 by showing the colocalization of TLR2 in glomeruli with synaptopodin, a podocyte marker, and Tie2, an endothelial marker. |
| 467 | 25715637 | In addition, proapoptotic molecules Bax and Caspase-3 were increased in the glomeruli of lipopolysaccharide-treated mice. |
| 468 | 25715637 | In addition, proapoptotic molecules Bax and Caspase-3 were increased in the glomeruli of lipopolysaccharide-treated mice. |
| 469 | 25715637 | Together, the current study indicates that TLR2 is overactivated in the glomerular endothelial cells and podocytes in septic AKI mice, while the abundance of Bax and Caspase-3 were increased in the glomeruli of these mice, it may supply a clue that TLR2 induced these cell apoptosis in AKI. |
| 470 | 25715637 | Together, the current study indicates that TLR2 is overactivated in the glomerular endothelial cells and podocytes in septic AKI mice, while the abundance of Bax and Caspase-3 were increased in the glomeruli of these mice, it may supply a clue that TLR2 induced these cell apoptosis in AKI. |
| 471 | 25284613 | Western blot analysis revealed that the protein expression of Bax and active fragments of caspase-3 were significantly increased, whereas phospho-Akt, β-catenin, and Bcl-2 protein expression were significantly decreased in DM glomeruli and HG-stimulated podocytes. |
| 472 | 25229402 | Furthermore, an obvious translocation of p-Smad3 from the cytosol to nuclei and induction of mitochondrial Nox4 were detected following PA application. |
| 473 | 25229402 | Induction of Nox4 by PA administration was significantly repressed by Smad3-shRNA, while Nox4-shRNA showed no effect on PA-induced p-Smad3 activation. |
| 474 | 25229402 | Notably, both Smad3 and Nox4 silencing significantly prevented the reduction of the mtDNA level, restored mitochondrial function, and decreased cellular apoptosis in PA-stimulated podocytes. |
| 475 | 25229402 | In conclusion, our findings demonstrated that Smad3-Nox4 axis-mediated mitochondrial dysfunction is involved in PA-induced podocyte damage likely via increasing ROS generation and activating the cytochrome c-caspase9-caspase3 apoptotic signaling pathway. |
| 476 | 25185988 | EGF receptor deletion in podocytes attenuates diabetic nephropathy. |
| 477 | 25185988 | EGF receptor deletion in podocytes attenuates diabetic nephropathy. |
| 478 | 25185988 | EGF receptor deletion in podocytes attenuates diabetic nephropathy. |
| 479 | 25185988 | In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. |
| 480 | 25185988 | In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. |
| 481 | 25185988 | In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFR(podKO)) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFR(podKO) mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. |
| 482 | 25185988 | Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFR(podKO) diabetic mice. |
| 483 | 25185988 | Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFR(podKO) diabetic mice. |
| 484 | 25185988 | Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFR(podKO) diabetic mice. |
| 485 | 25185988 | Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-β1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. |
| 486 | 25185988 | Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-β1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. |
| 487 | 25185988 | Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-β1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. |
| 488 | 25185988 | High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-β1, cleaved caspase 3, and Bcl2. |
| 489 | 25185988 | High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-β1, cleaved caspase 3, and Bcl2. |
| 490 | 25185988 | High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-β1, cleaved caspase 3, and Bcl2. |
| 491 | 24850187 | Podocytes count was evaluated by immunofluorescence staining and Wilms tumor 1 immunohistochemistry, and Western blot of nephrin and podocin. |
| 492 | 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. |
| 493 | 24815572 | The effect of albumin on podocytes: the role of the fatty acid moiety and the potential role of CD36 scavenger receptor. |
| 494 | 24815572 | Receptor-mediated endocytosis of FITC-HSA+FA over 60 min was 5 times greater than that of FITC-HSA-FA. 24h exposure of podocytes to albumin up-regulated nephrin expression and induced the activation of caspase-3. |
| 495 | 24815572 | Albumin endocytosis was enhanced in the presence of the CD36 specific inhibitor sulfo-N-succinimidyl oleate (SSO) while knock-down of CD36 using CD36siRNA had no effect on uptake. |
| 496 | 24566618 | Protection of human podocytes from shiga toxin 2-induced phosphorylation of mitogen-activated protein kinases and apoptosis by human serum amyloid P component. |
| 497 | 24566618 | Human serum amyloid P component (SAP), a member of the pentraxin family, has been shown to protect against Stx2-induced lethality in mice in vivo, presumably by specific binding to the toxin. |
| 498 | 24566618 | To elucidate the mechanisms underlying podocyte injury in HUS-associated proteinuria, we assessed Stx2-induced activation of mitogen-activated protein kinases (MAPKs) and apoptosis in immortalized human podocytes and evaluated the impact of SAP on Stx2-induced damage. |
| 499 | 24566618 | Stx2 applied to cultured podocytes was internalized and then activated p38α MAPK and c-Jun N-terminal kinase (JNK), important signaling steps in cell differentiation and apoptosis. |
| 500 | 24566618 | Stx2 also activated caspase 3, resulting in an increased level of apoptosis. |
| 501 | 24566618 | Coincubation of podocytes with SAP and Stx2 mitigated the effects of Stx2 and induced upregulation of antiapoptotic Bcl2. |
| 502 | 24566618 | These data suggest that podocytes are a target of Stx2 and that SAP protects podocytes against Stx2-induced injury. |
| 503 | 24337777 | We studied the effects of 3,4-DGE on cultured human podocytes and in vivo in mice. 3,4-DGE induced apoptosis in podocytes in a dose- and time-dependent manner. 3,4-DGE promoted the release of cytochrome c from mitochondria and activation of caspase-3. |
| 504 | 24337777 | We studied the effects of 3,4-DGE on cultured human podocytes and in vivo in mice. 3,4-DGE induced apoptosis in podocytes in a dose- and time-dependent manner. 3,4-DGE promoted the release of cytochrome c from mitochondria and activation of caspase-3. |
| 505 | 24337777 | Intravenous administration of 3,4-DGE to healthy mice resulted in a decreased expression of HSP27/HSPB1 and caspase-3 activation in whole kidney and in podocytes in vivo. |
| 506 | 24337777 | Intravenous administration of 3,4-DGE to healthy mice resulted in a decreased expression of HSP27/HSPB1 and caspase-3 activation in whole kidney and in podocytes in vivo. |
| 507 | 24259511 | Exogenous TGF-β1-induced podocyte apoptosis through caspase-3 activation, which was related to elevated ROS levels generated by selective upregulation of NADPH oxidase 4 (Nox4). |
| 508 | 24259511 | Exogenous TGF-β1-induced podocyte apoptosis through caspase-3 activation, which was related to elevated ROS levels generated by selective upregulation of NADPH oxidase 4 (Nox4). |
| 509 | 24259511 | Knockdown of either Smad2 or Smad3 prevented the increase of Nox4 expression, ROS generation, loss of mitochondrial membrane potential, and caspase-3 activation by TGF-β1. |
| 510 | 24259511 | Knockdown of either Smad2 or Smad3 prevented the increase of Nox4 expression, ROS generation, loss of mitochondrial membrane potential, and caspase-3 activation by TGF-β1. |
| 511 | 24259511 | These results suggest that TGF-β1-induced mitochondrial Nox4 upregulation via the TGF-β receptor-Smad2/3 pathway is responsible for ROS production, mitochondrial dysfunction, and apoptosis, which may at least in part contribute to the development and progression of proteinuric glomerular diseases such as diabetic nephropathy. |
| 512 | 24259511 | These results suggest that TGF-β1-induced mitochondrial Nox4 upregulation via the TGF-β receptor-Smad2/3 pathway is responsible for ROS production, mitochondrial dysfunction, and apoptosis, which may at least in part contribute to the development and progression of proteinuric glomerular diseases such as diabetic nephropathy. |
| 513 | 24117488 | Intraperitoneal administration of DXR (15 mg/kg, body weight, as a single dose) caused significant induction in the levels of angiotensin I, caspase-3, lactate dehydrogenase (LDH), lipid peroxidation malondialdehyde (MDA), urea, and creatinine. |
| 514 | 24117488 | Concomitant decline in the levels of albumin and total protein in plasma, reduction in reduced glutathione (GSH), and antiperoxidative enzyme superoxide dismutase (SOD) levels followed by ultrastructural alterations in the myocardial and renal tissues were also observed. |
| 515 | 23800993 | Apoptotic cell numbers, as measured by TUNEL staining and caspase 3 activity, were also augmented in the Ang II-treated group. |
| 516 | 23800993 | Pre-treatment with olmesartan (100 nmol/L, an Ang II type 1-receptor blocker), apocynin (50 μmol/L, NADPH oxidase inhibitor), or 5-N,N hexamethylene amiloride [30 μmol/L, Na⁺/H⁺ exchanger type 1 (NHE-1) inhibitor] abolished Ang II-induced podocyte apoptosis, whereas NHE-1 mRNA and protein expression was not affected by Ang II treatment. |
| 517 | 23800993 | Moreover, Ang II increased NHE-1 phosphorylation. |
| 518 | 23800993 | These results suggest that superoxide production, NHE-1 activation, and intracellular alkalization were early features prior to apoptosis in Ang II-treated mouse podocytes, and may offer new insights into the mechanisms responsible for Ang II-induced podocyte injury. |
| 519 | 23667252 | Yes-associated protein (YAP) promotes cell survival by inhibiting proapoptotic dendrin signaling. |
| 520 | 23667252 | Here we show that Yes-associated protein (YAP), a downstream target of Hippo kinases and an inhibitor of apoptosis, is expressed in the nucleus of podocytes. |
| 521 | 23667252 | This interaction is functionally relevant because YAP binding to dendrin reduces dendrin-dependent, staurosporine-induced apoptosis in co-transfected HEK293 cells. |
| 522 | 23667252 | It also increases staurosporine-induced caspase-3/7 activity, which is rescued by dendrin depletion in YAP knockdown cells. |
| 523 | 23667252 | Our findings elucidate YAP binding to dendrin as a prosurvival mechanism. |
| 524 | 23486009 | Prednisone reduced podocyte apoptosis measured by synaptopodin⁺/caspase-3⁺ double staining. |
| 525 | 23200848 | Inhibition of nephrin activation by c-mip through Csk-Cbp-Fyn axis plays a critical role in Angiotensin II-induced podocyte damage. |
| 526 | 23200848 | It has been demonstrated that nephrin inactivation plays a critical role in Angiotensin II (AngII)-induced podocyte damage both in in vitro and in vivo, but the underlying molecular mechanisms are still unclear. |
| 527 | 23200848 | In this study, the role of c-mip on AngII-induced nephrin inactivation and podocyte damage was explored in a mouse podocyte cell line. |
| 528 | 23200848 | In AngII stimulated podocyte, c-mip and Csk expressions increased obviously at protein level, and nephrin phosphorylation decreased while Cbp phosphorylation increased. |
| 529 | 23200848 | AngII-induced Csk increment and nephrin inactivation was remarkably inhibited by siCmip treatment. |
| 530 | 23200848 | AngII stimulation increased the interaction of c-mip and Csk, as well as Csk and Cbp. |
| 531 | 23200848 | Notably, the binding of Csk to active form pY418 decreased while the binding of Csk to inactive form pY530 of Src kinase Fyn increased in AngII-stimulated podocyte. |
| 532 | 23200848 | In addition, AngII stimulation significantly decreased the expression of phosphor-Akt (Ser473) and antiapoptotic protein Bcl-2, whereas increased the expression of apoptotic proteins caspase-3 and BAD, all of which were prevented by siCmip treatment. |
| 533 | 23200848 | Taken together, our results demonstrated that AngII induced nephrin inactivation and podocyte damage by the novel podocyte protein c-mip through Csk-Cbp-Fyn signaling pathway. |
| 534 | 22828802 | This effect of NMDA was associated with increased cell-surface expression of p47(phox), a cytosolic regulatory subunit of the NADPH oxidase NOX2. |
| 535 | 22828802 | NMDA treatment also evoked robust activation of Rho but not Rac,consistent with previous studies of downstream effectors of TRPC6 activation. |
| 536 | 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. |
| 537 | 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. |
| 538 | 22745830 | Apoptosis, albuminuria, ROS generation, caspase-3 activity and cleavage, as well as Bax and Bcl-2 mRNA and protein expression were measured in vitro and in vivo. |
| 539 | 22745830 | Apoptosis, albuminuria, ROS generation, caspase-3 activity and cleavage, as well as Bax and Bcl-2 mRNA and protein expression were measured in vitro and in vivo. |
| 540 | 22745830 | Apoptosis, albuminuria, ROS generation, caspase-3 activity and cleavage, as well as Bax and Bcl-2 mRNA and protein expression were measured in vitro and in vivo. |
| 541 | 22745830 | Apoptosis, albuminuria, ROS generation, caspase-3 activity and cleavage, as well as Bax and Bcl-2 mRNA and protein expression were measured in vitro and in vivo. |
| 542 | 22745830 | This antiapoptotic effect was associated with restoration of Bax and Bcl-2 expression, as well as inhibition of caspase-3 activation and overexpression. |
| 543 | 22745830 | This antiapoptotic effect was associated with restoration of Bax and Bcl-2 expression, as well as inhibition of caspase-3 activation and overexpression. |
| 544 | 22745830 | This antiapoptotic effect was associated with restoration of Bax and Bcl-2 expression, as well as inhibition of caspase-3 activation and overexpression. |
| 545 | 22745830 | This antiapoptotic effect was associated with restoration of Bax and Bcl-2 expression, as well as inhibition of caspase-3 activation and overexpression. |
| 546 | 22745830 | Increased apoptosis, Bax expression, caspase-3 activity and cleavage while decreased Bcl-2 expression were detected in diabetic rats. |
| 547 | 22745830 | Increased apoptosis, Bax expression, caspase-3 activity and cleavage while decreased Bcl-2 expression were detected in diabetic rats. |
| 548 | 22745830 | Increased apoptosis, Bax expression, caspase-3 activity and cleavage while decreased Bcl-2 expression were detected in diabetic rats. |
| 549 | 22745830 | Increased apoptosis, Bax expression, caspase-3 activity and cleavage while decreased Bcl-2 expression were detected in diabetic rats. |
| 550 | 22745830 | Expression of Bax and Bcl-2 mRNA and protein in kidney cortex was partially restored by AS-IV pretreatment. |
| 551 | 22745830 | Expression of Bax and Bcl-2 mRNA and protein in kidney cortex was partially restored by AS-IV pretreatment. |
| 552 | 22745830 | Expression of Bax and Bcl-2 mRNA and protein in kidney cortex was partially restored by AS-IV pretreatment. |
| 553 | 22745830 | Expression of Bax and Bcl-2 mRNA and protein in kidney cortex was partially restored by AS-IV pretreatment. |
| 554 | 22745830 | These findings suggested AS-IV, a novel antioxidant, to prevent Glucose-Induced podocyte apoptosis partly through restoring the balance of Bax and Bcl-2 expression and inhibiting caspase-3 activation. |
| 555 | 22745830 | These findings suggested AS-IV, a novel antioxidant, to prevent Glucose-Induced podocyte apoptosis partly through restoring the balance of Bax and Bcl-2 expression and inhibiting caspase-3 activation. |
| 556 | 22745830 | These findings suggested AS-IV, a novel antioxidant, to prevent Glucose-Induced podocyte apoptosis partly through restoring the balance of Bax and Bcl-2 expression and inhibiting caspase-3 activation. |
| 557 | 22745830 | These findings suggested AS-IV, a novel antioxidant, to prevent Glucose-Induced podocyte apoptosis partly through restoring the balance of Bax and Bcl-2 expression and inhibiting caspase-3 activation. |
| 558 | 22614921 | Considering that nestin is a substrate of cyclin-dependent kinase 5 (Cdk5), we further assessed the expression of Cdk5 in HG-treated podocytes. |
| 559 | 22614921 | The protein activator of Cdk5, p35, was also increased in a time-dependent manner by HG stimulation, and downregulation of Cdk5 by miRNA interference attenuated the nestin reduction in HG-treated podocytes; the HG-induced podocyte apoptosis, the increased cleaved caspase-3 expression and the Bax/Bcl-2 ratio were all effectively attenuated. |
| 560 | 22614921 | These data suggested that nestin, which is dependent on Cdk5 regulation, plays a cytoprotective role in HG-induced podocyte apoptosis. |
| 561 | 22270613 | Leukemia inhibitory factor (LIF) is a pleiotropic glycoprotein belonging to the interleukin-6 family of cytokines. |
| 562 | 22270613 | The measurement of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, superoxide dismutase (SOD), malondialdehyde (MDA), and caspase-3 activity levels showed that LIF attenuated the high glucose-induced decreased level of SOD and elevated level of NADPH oxidase, MDA and caspase-3 activity. |
| 563 | 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. |
| 564 | 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. |
| 565 | 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. |
| 566 | 21368746 | In cultured podocytes, DOX induced apoptosis, increased cleaved caspase-3 levels, and decreased Bcl-2 expression, all attenuated by pretreatment with fenofibrate. |
| 567 | 21289056 | In addition, there was greater apoptosis (cleaved caspase-3 immunostaining), fewer podocytes (Wilms' tumor-1 immunostaining), and less proliferation (Ki-67 immunostaining) in diseased SM22α +/+ mice. |
| 568 | 21269661 | The effects of angiotensin-II receptor blockers on podocyte damage and glomerular apoptosis in a rat model of experimental streptozotocin-induced diabetic nephropathy. |
| 569 | 21269661 | The effects of angiotensin-II receptor blockers on podocyte damage and glomerular apoptosis in a rat model of experimental streptozotocin-induced diabetic nephropathy. |
| 570 | 21269661 | The aim of the study was to determine in a rat model of streptozotocin-induced diabetic nephropathy the expression of: WT-1 (for podocyte loss in the glomerulus), TGF-beta 1 (for tissue damage), caspase-3 and bax (for glomerular apoptosis) and the possible protective effects of an angiotensin II type 1 receptor blocker. |
| 571 | 21269661 | The aim of the study was to determine in a rat model of streptozotocin-induced diabetic nephropathy the expression of: WT-1 (for podocyte loss in the glomerulus), TGF-beta 1 (for tissue damage), caspase-3 and bax (for glomerular apoptosis) and the possible protective effects of an angiotensin II type 1 receptor blocker. |
| 572 | 21269661 | We conclude that the decrease in the number of podocytes is an early marker of diabetic nephropathy, AT1 receptor blocker has renoprotective effects on the regulation of renal hemodynamics and on the control of tissue damage by preventing podocyte loss, which leads to decrease of bax and caspase-3 expressions of apoptosis related proteins, and may prevent glomerular cell apoptosis via angiotensin II. |
| 573 | 21269661 | We conclude that the decrease in the number of podocytes is an early marker of diabetic nephropathy, AT1 receptor blocker has renoprotective effects on the regulation of renal hemodynamics and on the control of tissue damage by preventing podocyte loss, which leads to decrease of bax and caspase-3 expressions of apoptosis related proteins, and may prevent glomerular cell apoptosis via angiotensin II. |
| 574 | 20017105 | We assessed renal allograft biopsies from DGF patients treated with de novo sirolimus (n = 10) for renal tubular cell and podocyte apoptosis and expression of activated caspase-3, Bcl-2, and mTOR and compared them to biopsies from DGF patients not receiving sirolimus (n = 15). |
| 575 | 20017105 | We assessed renal allograft biopsies from DGF patients treated with de novo sirolimus (n = 10) for renal tubular cell and podocyte apoptosis and expression of activated caspase-3, Bcl-2, and mTOR and compared them to biopsies from DGF patients not receiving sirolimus (n = 15). |
| 576 | 20017105 | We assessed renal allograft biopsies from DGF patients treated with de novo sirolimus (n = 10) for renal tubular cell and podocyte apoptosis and expression of activated caspase-3, Bcl-2, and mTOR and compared them to biopsies from DGF patients not receiving sirolimus (n = 15). |
| 577 | 20017105 | We assessed renal allograft biopsies from DGF patients treated with de novo sirolimus (n = 10) for renal tubular cell and podocyte apoptosis and expression of activated caspase-3, Bcl-2, and mTOR and compared them to biopsies from DGF patients not receiving sirolimus (n = 15). |
| 578 | 20017105 | Caspase-3, Bcl-2, and mTOR expression were assessed by immunohistochemistry. |
| 579 | 20017105 | Caspase-3, Bcl-2, and mTOR expression were assessed by immunohistochemistry. |
| 580 | 20017105 | Caspase-3, Bcl-2, and mTOR expression were assessed by immunohistochemistry. |
| 581 | 20017105 | Caspase-3, Bcl-2, and mTOR expression were assessed by immunohistochemistry. |
| 582 | 20017105 | Expression of activated caspase-3, Bcl-2, or activated mTOR did not differ between groups. 60% of biopsies from sirolimus treated patients compared to 7% of biopsies from controls showed diffuse podocyte apoptosis (p = 0.007). |
| 583 | 20017105 | Expression of activated caspase-3, Bcl-2, or activated mTOR did not differ between groups. 60% of biopsies from sirolimus treated patients compared to 7% of biopsies from controls showed diffuse podocyte apoptosis (p = 0.007). |
| 584 | 20017105 | Expression of activated caspase-3, Bcl-2, or activated mTOR did not differ between groups. 60% of biopsies from sirolimus treated patients compared to 7% of biopsies from controls showed diffuse podocyte apoptosis (p = 0.007). |
| 585 | 20017105 | Expression of activated caspase-3, Bcl-2, or activated mTOR did not differ between groups. 60% of biopsies from sirolimus treated patients compared to 7% of biopsies from controls showed diffuse podocyte apoptosis (p = 0.007). |
| 586 | 20017105 | There was no podocyte expression of activated mTOR, activated caspase-3, or Bcl-2 in either group. |
| 587 | 20017105 | There was no podocyte expression of activated mTOR, activated caspase-3, or Bcl-2 in either group. |
| 588 | 20017105 | There was no podocyte expression of activated mTOR, activated caspase-3, or Bcl-2 in either group. |
| 589 | 20017105 | There was no podocyte expression of activated mTOR, activated caspase-3, or Bcl-2 in either group. |
| 590 | 19727064 | Increasing the amount of AOPPs in the media of conditionally immortalized podocytes rapidly triggered the production of intracellular superoxide by activation of NADPH oxidase and this, in turn, led to an upregulation of p53, Bax, caspase 3 activity, and apoptosis. |
| 591 | 19710242 | Aldosterone synthase (CYP11B2) and MCR mRNA and protein expression were determined by real-time PCR and Western blot, respectively, and aldosterone levels by radioimmunoassay. |
| 592 | 19710242 | CYP11B2 and MCR expression were significantly higher in HG-stimulated podocytes and DM glomeruli compared with NG cells and C glomeruli, respectively, along with increased aldosterone levels. |
| 593 | 19710242 | Western blot analysis revealed that cleaved caspase-3 and Bax expression was significantly increased, whereas Bcl-2 expression was significantly decreased in HG-stimulated podocytes and in DM glomeruli. |
| 594 | 19657327 | HO-1 expression, its activity, the ratio of Bax/Bcl-2 protein, and active caspase-3 fragments were all significantly higher in isolated glomeruli of diabetic rats and in high glucose-treated podocytes. |
| 595 | 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. |
| 596 | 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)]. |
| 597 | 17804487 | HG as well as TGF-beta raise caspase-3 activity, increase apoptosis, and reduce cell survival which is, in part, blocked by BMP7. |
| 598 | 17804487 | Knockdown and forced expression studies indicate that smad5 is required as well as sufficient for these actions of BMP7. |
| 599 | 17804487 | These findings indicate that BMP7 is a differentiation and survival factor for podocytes, requires smad5, and can reduce diabetic podocyte injury. |
| 600 | 17457378 | The PPAR-gamma agonist significantly restored expression of the cyclin-dependent kinase inhibitor p27 and the antiapoptotic molecule Bcl-xL while significantly decreasing proapoptotic caspase-3 activity. |
| 601 | 17457378 | We postulate that this protective effect may be mediated in part by effects on p27 and TGF-beta expression. |
| 602 | 16380497 | Increased extracellular glucose (30 mmol/l) rapidly stimulated generation of intracellular reactive oxygen species (ROS) through NADPH oxidase and mitochondrial pathways and led to activation of proapoptotic p38 mitogen-activated protein kinase and caspase 3 and to apoptosis of conditionally immortalized podocytes in vitro. |
| 603 | 15987750 | Dexamethasone prevents podocyte apoptosis induced by puromycin aminonucleoside: role of p53 and Bcl-2-related family proteins. |
| 604 | 15987750 | Dexamethasone also lowered the increase in the proapoptotic Bax, which was increased by PA, and increased expression of the antiapoptotic Bcl-xL protein. |
| 605 | 15987750 | Moreover, the decrease in p53 by dexamethasone was associated with increased Bcl-xL levels. |
| 606 | 15987750 | Podocyte apoptosis induced by PA was caspase-3 independent but was associated with the translocation of apoptosis-inducing factor (AIF) from the cytoplasm to nuclei. |
| 607 | 15987750 | These results show that PA-induced podocyte apoptosis is p53 dependent and associated with changes in Bcl-2-related proteins and AIF translocation. |
| 608 | 15987750 | The protective effects of dexamethasone on PA-induced apoptosis were associated with decreasing p53, increasing Bcl-xL, and inhibition of AIF translocation. |
| 609 | 11560950 | Apoptosis in podocytes induced by TGF-beta and Smad7. |
| 610 | 11560950 | TGF-beta1 and Smad7 each induce apoptosis in podocytes, and their coexpression has an additive effect. |
| 611 | 11560950 | Activation of p38 MAP kinase and caspase-3 is required for TGF-beta-mediated apoptosis, but not for apoptosis induced by Smad7. |
| 612 | 11560950 | Unlike TGF-beta, Smad7 inhibits nuclear translocation and transcriptional activity of the cell survival factor NF-kappaB. |