scholarly journals miR-141 regulates TGF-β1-induced epithelial-mesenchymal transition through repression of HIPK2 expression in renal tubular epithelial cells

2014 ◽  
Vol 35 (2) ◽  
pp. 311-318 ◽  
Author(s):  
YUANHANG HUANG ◽  
JUNRONG TONG ◽  
FENG HE ◽  
XINPEI YU ◽  
LIMING FAN ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Tgf Β1

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.

scholarly journals Effect of Huai Qi Huang on Epithelial-Mesenchymal Transition of Renal Tubular Epithelial Cells through miR-200a

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Jinyun Pu ◽  
Yu Zhang ◽  
Jianhua Zhou
Keyword(s):  
Epithelial Cells ◽  
Molecular Mechanism ◽  
Renal Fibrosis ◽  
Epithelial Mesenchymal Transition ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Renal Tubular

Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells is a vital mechanism of renal fibrosis. Mounting evidence suggests that miR-200a expression decreases in tubular epithelial cells in unilateral ureteral obstruction (UUO) rats. Moreover, it has been demonstrated that Huai Qi Huang (HQH) can ameliorate tubulointerstitial damage in adriamycin nephrosis and delay kidney dysfunction in primary glomerular disease. However, the effect of HQH on EMT of tubular epithelial cells in UUO rats and its molecular mechanism is unclear. In order to explore the effect of HQH on EMT and its molecular mechanism in renal fibrosis,in vitroandin vivoexperiments were performed in our study. Our results showed that HQH increased miR-200a expression in UUO rats and in TGF-β1 stimulated NRK-52E cells. Meanwhile, HQH decreased ZEB1 and ZEB2 (the transcriptional repressors of E-cadherin),α-SMA expression in renal tubular epithelial cellsin vitroandin vivo. Furthermore, we found that HQH protected kidney from fibrosis in UUO rats. The results demonstrated that HQH regulated miR-200a/ZEBs pathway and inhibited EMT process, which may be a mechanism of protecting effect on tubular cells in renal fibrosis.

Sign in / Sign up

Export Citation Format

Share Document