scholarly journals MicroRNA‑101 inhibits renal tubular epithelial‑to‑mesenchymal transition by targeting TGF‑β1 type I receptor

2021 ◽  
Vol 47 (6) ◽  
Author(s):  
Qinglan Wang ◽  
Yanyan Tao ◽  
Hongdong Xie ◽  
Chenghai Liu ◽  
Ping Liu
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Type I ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Tgf Β1

scholarly journals Niaoduqing Granules Inhibits TGF-β1-induced Epithelial-Mesenchymal Transition in Human Renal Tubular Epithelial HK-2 Cells

2020 ◽  
Author(s):  
Chu-Ying Huo ◽  
Hua-Yi Yang ◽  
Wei-Min Ning ◽  
Lin-Zhong Yu ◽  
Chun-Lin Fan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Morphological Changes ◽  
Migration And Invasion ◽  
Type I ◽  
Mesenchymal Transition ◽  
Public Health Burden ◽  
Fluorescence Confocal Microscopy ◽  
Renal Tubular ◽  
Tgf Β1

Abstract Background: Chronic renal failure (CRF) is a worldwide public health burden. Niaoduqing granules (NDQ) is widely used for CRF treatment in China. However, the underlying mechanism of NDQ is not fully studied. This study is aimed to investigate whether NDQ ameliorate CRF by inhibiting TGF-β1-induced EMT in human renal tubular epithelial HK-2 cells.Methods: MTT assay and colony formation assay were used to investigate the cytotoxicity of NDQ in HK-2 cells. Morphological changes of HK-2 cells after TGF-β1 or/and NDQ treatment were observed under a microscope. Wound-healing, migration and invasion assays were performed to determine the cell movement, migratory and invasive abilities, respectively. Western blot analysis was carried out to examine the protein levels of TGF-β type I receptor (TβRI) and EMT-associated factors. Fluorescence confocal microscopy was applied to observe the organization of F-actin.Results: NDQ suppressed TβRI expression dose-dependently. NDQ inhibited TGF-β1-stimulated EMT in HK-2 cells, supported by the evidences that NDQ prevented morphology change, attenuated cell migration and invasion, downregulated EMT factors and reorganized F-actin distribution in TGF-β1-stimulated HK-2 cells.Conclusions: NDQ attenuates chronic renal failure which may be associated with inhibition of TβRI expression and EMT process.

The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression

2012 ◽  
Vol 302 (3) ◽  
pp. F369-F379 ◽  
Author(s):  
Mingxia Xiong ◽  
Lei Jiang ◽  
Yang Zhou ◽  
Wenjing Qiu ◽  
Li Fang ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Expression Profiles ◽  
Renal Tubules ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Novel Therapeutic Strategies ◽  
Tgf Β1

Most chronic kidney injuries inevitably progress to irreversible renal fibrosis. Tubular epithelial-to-mesenchymal transition (EMT) is recognized to play pivotal roles in the process of renal fibrosis. However, a comprehensive understanding of the pathogenesis of renal scar formation and progression remains an urgent task for renal researchers. The endogenously produced microRNAs (miRNAs), proved to play important roles in gene regulation, probably regulate most genes involved in EMT. In this study, we applied microarray analysis to investigate the expression profiles of miRNA in murine interstitial fibrotic kidneys induced by unilateral ureteral obstruction (UUO). It was found that miR-200a and miR-141, two members of the miR-200 family, were downregulated at the early phase of UUO. In TGF-β1-induced tubular EMT in vitro, it was also found that the members of the miR-200 family were downregulated in a Smad signaling-dependent manner. It was demonstrated that the miR-200 family was responsible for protecting tubular epithelial cells from mesenchymal transition by target suppression of zinc finger E-box-binding homeobox (ZEB) 1 and ZEB2, which are E-cadherin transcriptional repressors. The results suggest that downregulation of the miR-200 family initiates the dedifferentiation of renal tubules and progression of renal fibrosis, which might provide important targets for novel therapeutic strategies.

Focal adhesion kinase mediates TGF-β1-induced renal tubular epithelial-to-mesenchymal transition in vitro

2010 ◽  
Vol 340 (1-2) ◽  
pp. 21-29 ◽  
Author(s):  
Bingqing Deng ◽  
Xiao Yang ◽  
Jianshe Liu ◽  
Fangfang He ◽  
Zhonghua Zhu ◽  
...  
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Renal Tubular ◽  
Tgf Β1

scholarly journals Metformin Improves Epithelial-to-Mesenchymal Transition Induced by TGF-β1 in Renal Tubular Epithelial NRK-52E Cells via Inhibiting Egr-1

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Meiping Guan ◽  
Wenqi Li ◽  
Lingling Xu ◽  
Yanmei Zeng ◽  
Dan Wang ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Mesenchymal Transition ◽  
Early Growth Response ◽  
Real Time Quantitative Pcr ◽  
Novel Target ◽  
Renal Tubular ◽  
Tgf Β1 ◽  
E Cadherin

The early growth response- (Egr-) 1 has been found to play a key role in organ fibrosis. Metformin has been shown to be effective in attenuating renal tubular epithelial-to-mesenchymal transition (EMT), which is involved in renal fibrosis. However, it is unknown whether metformin improves EMT via inhibiting Egr-1. In this study, rat renal tubular epithelial (NRK-52 E) cells, treated by transforming growth factor- (TGF-)β1 of 10 ng/ml with or without metformin of 1 mmol/l, were transfected by siEgr-1 or M61-Egr-1 plasmids to knock down or overexpress Egr-1, respectively. The gene and protein expressions of E-cadherin,α-SMA, fibronectin (FN), and Egr-1 were determined by real-time quantitative PCR and Western blotting, respectively. We observed that TGF-β1 significantly reduced E-cadherin expression and upregulated the expressions of FN,α-SMA, and Egr-1, which can be reversed by metformin. M61-Egr-1 transfection could exacerbate EMT, which can be reversed by metformin. Taken together, our data show that Egr-1 plays an important role in TGF-β1-induced EMT of renal tubular epithelial cells and metformin improves EMT while inhibiting Egr-1, which provides a potential novel target to combat renal fibrosis.

Sign in / Sign up

Export Citation Format

Share Document