Formin mDia1 contributes to migration and epithelial‐mesenchymal transition of tubular epithelial cells exposed to TGF‐β1

2019 ◽  
Vol 121 (8-9) ◽  
pp. 3861-3870 ◽  
Author(s):  
Yu‐Ying Li ◽  
Guo‐Tao Jiang ◽  
Li‐Jie Chen ◽  
Yan‐Hong Jiang ◽  
Jun‐Dong Jiao
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Tgf Β1

Lefty antagonises TGF-β1 induced epithelial–mesenchymal transition in tubular epithelial cells

2010 ◽  
Vol 393 (4) ◽  
pp. 855-859 ◽  
Author(s):  
Mythily Mariasegaram ◽  
Greg H. Tesch ◽  
Sarah Verhardt ◽  
Lyn Hurst ◽  
Hui Y. Lan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Tgf Β1

scholarly journals Promotion of USP4 to TGF-β1-induced EMT in renal tubular epithelial cells is regulated by Akt through stabilizing TβRI

2020 ◽  
Author(s):  
Jin-Yun Pu ◽  
Li-Xia Wang ◽  
Jie Wang ◽  
Yu Zhang ◽  
Jian-Hua Zhou
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Renal Fibrosis ◽  
Epithelial Mesenchymal Transition ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Pi3k Inhibitor Ly294002 ◽  
Tgf Β1 ◽  
E Cadherin

AbstractObjectiveWe aimed to explore the role of ubiquitin-specific peptidase-4 (USP4) in TGF-β1 induced epithelial-mesenchymal transition (EMT) during renal fibrosis, and investigated that if Akt inactivation exerted a critical effect on EMT via USP4/TβRI pathway.MethodsUSP4, pAkt and TβRI proteins in the obstructed kidneys from unilateral ureteral obstruction (UUO) rats were detected by immunohistochemistry assay or western blot method. E-cadherin, α-SMA, USP4 and pAkt protein expression in NRK-52E cells at different concentration of TGF-β1 were detected at different time. Further, NRK-52E cells were transfected with USP4-specific siRNA (si-USP4), and then stimulated with 10 ng/ml TGF-β1 for 24h to detect E-cadherin, α-SMA, E-cadherin and TβRI by immunofluorescent double staining assay. Pretreated with PI3K inhibitor LY294002, protein expression levels of pAkt, E-cadherin, α-SMA were detected. Meanwhile, the location of USP4 was visualized by immunofluorescent assay in NRK-52E cells.ResultsThe expression of USP4 and TβRI was significantly upregulated in the tubular epithelial cells of UUO rats. We also found that TGF-β1 upregulated USP4 and activated Akt in NRK-52E cells during EMT. In vitro, downregulation of USP4 inhibited TβRI expression and partially reversed EMT stimulated by TGF-β1. In the meantime, blunted phosphorylation of Akt with LY294002 promoted the E-cadherin expression, and inhibited α-SMA expression in response to TGF-β1. However, inactivation of Akt could reverse EMT process, but failed to induce USP4 to shuttle between the nucleus and the cytoplasm in NRK-52E cells stimulated by TGF-β1.ConclusionsThese data implied that USP4 was a harmful molecule induced by TGF-β1, regulated by Akt activation and promoted TGF-β1-induced EMT via TβRI in tubular epithelial cells during renal fibrosis.

IGFBP7 regulates sepsis-induced epithelial-mesenchymal transition through ERK1/2 signaling

2019 ◽  
Vol 51 (8) ◽  
pp. 799-806
Author(s):  
Xiaolin Wang ◽  
Yan Li ◽  
Zhenzhen Zhao ◽  
Yan Meng ◽  
Jinjun Bian ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Hk2 Cells ◽  
Tgf Β1

Abstract The epithelial-mesenchymal transition (EMT) process results in fibrosis of renal tubular epithelial cells and is of great importance in the development of acute kidney injury (AKI). Urinary IGF-binding protein-7 (IGFBP7) was obviously increased in AKI and is considered to be a biomarker for AKI. However, whether it has an effect on the inhibition of lipopolysaccharide (LPS)-induced EMT in human HK2 cells and on that of cecal ligation and puncture (CLP)-induced EMT in human HK2 cells and in mice remains to be elucidated. Western blot analysis was performed to examine the phosphorylation of ERK1/2 level and expressions of IGFBP7, ERK1/2, EMT markers, such as E-cadherin, α-SMA, and vimentin, and EMT regulatory factors, such as Snail, transforming growth factor-β1 (TGF-β1), and connective tissue growth factor (CTGF). The levels of IGFBP7, TGF-β1, and CTGF were detected by enzyme linked immunosorbent assay (ELISA). Concentrations of creatinine (Cr), blood urea nitrogen (BUN), and albumin (ALB) were measured by biochemical analysis. Here, we found that LPS promoted EMT and ERK1/2 activation in HK2 cells, which were inhibited by silencing of IGFBP7. Furthermore, IGFBP7 overexpression significantly increased EMT and ERK1/2 activation in HK2 cells, which were inhibited by ERK1/2 signaling inhibitor PD98059. IGFBP7 knockdown effectively attenuated renal fibrosis, concentrations of Cr, BUN and ALB, and activation of ERK1/2 signaling in CLP-induced mice. These results suggest that inhibiting IGFBP7 can effectively protect the renal tubular epithelial cells from EMT induced by LPS or CLP both in vitro and in vivo, which may be associated with inactivation of ERK1/2 signaling.

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