Objective: To explore the regulatory role of miR-1908 in renal fibrosis.
Methods: The level of miR-1908 and transforming growth factor beta 1 (TGF-β1) mRNA during renal fibrosis were detected with real-time quantitative PCR. Bioinformatics and luciferase reporter gene analyses were applied to determine the targeting relationship between miR-1908 and TGF-β1 mRNA. After primary human renal interstitial fibroblasts were transfected with miR-1908 adenoviral expression vector in vitro, Western blotting was used to detect the protein levels of TGF-β1, smad2/3 and matrix metalloproteinase 2 (MMP-2) in the cells. Six weeks after intraperitoneal injection of miR-1908 adenoviral vector, the renal tissue sections of the renal fibrosis mouse models were stained with Masson staining.
Results: Human miR-1908 showed a gradually decreasing expression during renal fibrosis process, which was completely contrary to the changes of TGF-β1 mRNA. Overexpression of miR-1908 suppressed the expressions of TGF-β1, smad2/3 and MMP-2 in human primary renal interstitial cells. The renal fibrosis was significantly relieved in the mice injected with miR-1908 adenovirus vector injection compared with the ones without injection.
Conclusion: miR-1908 could inhibit renal fibrosis through targeting TGF-β1.