Transforming growth factor β1 induced human proximal tubular epithelial cells to produce stem cell factor

2010 ◽  
Vol 34 (8) ◽  
pp. S3-S3
Author(s):  
Xuemei Liu ◽  
Aihua Yang ◽  
Xu Yan ◽  
Ruixia Ma ◽  
Liqiu Liu
Keyword(s):  
Stem Cell ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Stem Cell Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tubular Epithelial Cells ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular

scholarly journals TMEM88 inhibits fibrosis in renal proximal tubular epithelial cells by suppressing the transforming growth factor-β1/Smad signaling pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 6928-6934 ◽  
Author(s):  
Huicong Li ◽  
Yunqian Wang ◽  
Baoping Chen ◽  
Jun Shi
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Transmembrane Protein ◽  
Transforming Growth Factor Β1 ◽  
Tubular Epithelial Cells ◽  
Smad Signaling Pathway ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Transmembrane protein 88 (TMEM88) belongs to a member of the TMEM family, and was reported to be involved in fibrogenesis.

scholarly journals Retraction: TMEM88 inhibits fibrosis in renal proximal tubular epithelial cells by suppressing the transforming growth factor-β1/Smad signaling pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 5019-5019
Author(s):  
Laura Fisher
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tubular Epithelial Cells ◽  
Smad Signaling Pathway ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Renal Proximal Tubular

Retraction of ‘TMEM88 inhibits fibrosis in renal proximal tubular epithelial cells by suppressing the transforming growth factor-β1/Smad signaling pathway’ by Huicong Li et al., RSC Adv., 2019, 9, 6928–6934, DOI: 10.1039/C8RA10369K.

V-ATPase promotes transforming growth factor-β-induced epithelial-mesenchymal transition of rat proximal tubular epithelial cells

2012 ◽  
Vol 302 (9) ◽  
pp. F1121-F1132 ◽  
Author(s):  
Xueqin Cao ◽  
Qiongqiong Yang ◽  
Jing Qin ◽  
Shili Zhao ◽  
Xiaoyan Li ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Transforming Growth Factor ◽  
Tubulointerstitial Fibrosis ◽  
Dependent Manner ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Proximal Tubular Epithelial Cells ◽  
Proximal Tubular ◽  
Tgf Β1

The ubiquitous vacuolar H+-ATPase (V-ATPase), a multisubunit proton pump, is essential for intraorganellar acidification. Here, we hypothesized that V-ATPase is involved in the pathogenesis of kidney tubulointerstitial fibrosis. We first examined its expression in the rat unilateral ureteral obstruction (UUO) model of kidney fibrosis and transforming growth factor (TGF)-β1-mediated epithelial-to-mesenchymal transition (EMT) in rat proximal tubular epithelial cells (NRK52E). Immunofluorescence experiments showed that UUO resulted in significant upregulation of V-ATPase subunits (B2, E, and c) and α-smooth muscle actin (α-SMA) in areas of tubulointerstitial injury. We further observed that TGF-β1 (10 ng/ml) treatment resulted in EMT of NRK52E (upregulation of α-SMA and downregulation of E-cadherin) in a time-dependent manner and significant upregulation of V-ATPase B2 and c subunits after 48 h and the E subunit after 24 h, by real-time PCR and immunoblot analyses. The ATP hydrolysis activity tested by an ATP/NADH-coupled assay was increased after 48-h TGF-β1 treatment. Using intracellular pH measurements with the SNARF-4F indicator, Na+-independent pH recovery was significantly faster after an NH4Cl pulse in 48-h TGF-β1-treated cells than controls. Furthermore, the V-ATPase inhibitor bafilomycin A1 partially protected the cells from EMT. TGF-β1 induced an increase in the cell surface expression of the B2 subunit, and small interfering RNA-mediated B2 subunit knockdown partially reduced the V-ATPase activity and attenuated EMT induced by TGF-β1. Together, these findings show that V-ATPase may promote EMT and chronic tubulointerstitial fibrosis due to increasing its activity by either overexpression or redistribution of its subunits.

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