Expression of miR-207 in renal tissue of renal fibrosis rats and its correlation analysis with protein expression of TGF-β1 and Smad3

OBJECTIVE: This study was designed to analyze the expression of miR-207 in renal tissue of renal fibrosis rats and its correlation with the protein expression of TGF-beta 1 and Smad3. MATERIALS AND METHODS: Rat models with renal fibrosis were established via unilateral ureteral obstruction (UUO). Then, the expression levels of miR-207, TGF-beta 1 and Smad3 in renal tissue of rats were intervened by over-expression vector miR-207 mimic, miR-207 inhibitor and TGF-beta/Smad3 signal SIS3 free base, and the effect and mechanism of action of miR-207 on renal fibrosis were analyzed. RESULTS: In UUO models established in this study, the expression levels of fibrosis related factors TGF-beta 1, Smad3. Smad2, alpha-SMA. BMP-7, MMP7 and MMP9 were elevated, and staining results showed that obvious fibrosis occurred in renal tissue of rats. Moreover, we also found that the miR-207 expression increased in UUO model rats. After inhibiting miR-207 expression, their degree of renal fibrosis also reduced significantly. and the expression levels of TGF-beta 1, Smad3. Smad2. alpha-SMA. BMP-7. MMP7 and MMP9 were inhibited. Besides, miR-207 had a positive correlation with TGF-beta 1/Smad3 expression. We designed a group of rats, and found that while miR-207 expression was up-regulated, TGF-beta 1/ Smad3 signals were inhibited, and compared with those with up-regulation of miR-207 expression, the severity of renal fibrosis reduced significantly, and the expression of other fibrosis indicators Smad2, alpha-SMA, BMP-7, MMP7 and MMP9 also reduced dramatically. CONCLUSIONS: The miR-207 expression in renal tissue of rats with renal fibrosis increased, which was positively correlated with TGF-beta 1/Smad3, and miR-207 could promote the progression of renal fibrosis through TGF-beta 1/Smad3 signals.

Automated summary

The study found that miR-207 expression was positively correlated with the severity of renal fibrosis, and miR-207 promoted the progression of renal fibrosis through the TGF-beta 1/Smad3 signals.