LncRNA GAS5 exacerbates renal tubular epithelial fibrosis by acting as a competing endogenous RNA of miR-96-5p - 30/11/19
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Highlights |
• | GAS5 is a lncRNA that was identified to be notably increased in renal tissues of DKD mice and TGF-β1-induced HK-2 cells. |
• | Our data enriched the research of lncRNA GAS5 and miR-96-5p, confirming their role in TGF-β1-induced renal tubular injury. |
• | Our study demonstrates that knockdown of lncRNA GAS5 led to antifibrosis by competitively binding miR-96-5p, which inhibited the expression of FN1. These results indicate that targeting LncRNA GAS5 may be a promising therapeutic strategy for preventing diabetic kidney injury. |
Abstract |
Renal fibrosis is at the core of various renal diseases, including diabetic kidney disease (DKD). Long noncoding RNAs (lncRNAs) are known players in the regulation of renal fibrosis. However, their expression and function in DKD still need to be elucidated. The purpose of this study was to assess how lncRNA GAS5 regulates fibrosis and its mechanism in TGF-β1-treated renal proximal tubular cell.In this study, the lncRNA GAS5 was upregulated in both TGF-β1-treated HK-2 cells and the kidneys of HDF/STZ mice. Knockdown of GAS5 relieved renal tubular epithelial fibrosis. This effect was mediated by the downregulation and functional inactivation of miR-96-5p. Furthermore, miR-96-5p was downregulated in DKD mice, and this downregulation attenuated the repression of FN1(fibronectin, FN) and led to its upregulation. The decrease in miR-96-5p was partially attributed to the miRNA-sponge action of GAS5.Our research demonstrates that knockdown of lncRNA GAS5 leads to antifibrosis by competitively binding miR-96-5p, which inhibits the expression of FN1. These results indicate that targeting lncRNA GAS5 may be a promising therapeutic strategy for preventing DKD.
Le texte complet de cet article est disponible en PDF.Keywords : Diabetic kidney disease, Renal fibrosis, HK-2, miR-96-5p, lncRNA, GAS
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