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MiR-150-5p Alleviates Renal Tubule Epithelial Cell Fibrosis via the Inhibition of Epithelial-Mesenchymal Transition
Zhizhong Zhang1, Xinyu Zhang2, Xiangming Gao3
1Department of Urology, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan, China.
Introduction:
Although microRNA (miR)-150-5p participates in the progression of renal fibrosis, its mechanism of action remains elusive.
Methods:
A mouse model of unilateral ureteral obstruction was used. The in vitro renal fibrosis model was established by stimulating human kidney 2 (HK-2) cells with transforming growth factor beta 1 (TGF-β1). The expression profiles of miR-150-5p, zinc finger E-box binding homeobox 1 (ZEB1), and other fibrosis- and epithelial-mesenchymal transition (EMT)-linked proteins were determined using Western blot and quantitative reverse transcription polymerase chain reaction. The relationship between miR-150-5p and ZEB1 in HK-2 cells was confirmed by a dual-luciferase reporter assay.
Results:
Both in vivo and in vitro renal fibrosis models revealed reduced miR-150-5p expression and elevated ZEB1 level. A significant decrease in E-cadherin levels, as well as increases in alpha smooth muscle actin (α-SMA) and collagen type I (Col-I) levels, was seen in TGF-β1-treated HK-2 cells. The overexpression of miR-150-5p ameliorated TGF-β1-mediated fibrosis and EMT. Notably, miR-150-5p acts by directly targeting ZEB1. A significant reversal of the inhibitory impact of miR-150-5p on TGF-β1-mediated fibrosis and EMT in HK-2 cells was observed upon ZEB1 overexpression.
Conclusion:
MiR-150-5p suppresses TGF-β1-induced fibrosis and EMT by targeting ZEB1 in HK-2 cells, providing helpful insights into the therapeutic intervention of renal fibrosis.
Insights
MicroRNA (miR)-150-5p suppresses kidney fibrosis by targeting ZEB1. This finding offers new therapeutic strategies for renal fibrosis by modulating miR-150-5p and ZEB1 interactions.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- MicroRNA (miR)-150-5p is implicated in renal fibrosis progression.
- The precise mechanism of miR-150-5p in renal fibrosis remains unclear.
Purpose of the Study:
- To elucidate the role and mechanism of miR-150-5p in transforming growth factor beta 1 (TGF-β1)-induced renal fibrosis and epithelial-mesenchymal transition (EMT).
Main Methods:
- Utilized a mouse model of unilateral ureteral obstruction and an in vitro model using human kidney 2 (HK-2) cells stimulated with TGF-β1.
- Assessed expression of miR-150-5p, zinc finger E-box binding homeobox 1 (ZEB1), and fibrosis/EMT markers via Western blot and qRT-PCR.
- Confirmed the miR-150-5p and ZEB1 interaction using a dual-luciferase reporter assay.
Main Results:
- Renal fibrosis models showed decreased miR-150-5p and increased ZEB1.
- TGF-β1 treatment induced EMT markers (decreased E-cadherin, increased α-SMA and Col-I) in HK-2 cells.
- miR-150-5p overexpression inhibited TGF-β1-induced fibrosis and EMT, acting via direct targeting of ZEB1. ZEB1 overexpression reversed these effects.
Conclusions:
- MiR-150-5p exerts a protective effect against TGF-β1-induced renal fibrosis and EMT by directly targeting ZEB1 in HK-2 cells.
- This study provides a mechanistic understanding that could inform therapeutic strategies for renal fibrosis.
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