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Background and Aims The aim of the present study was to investigate the molecular mechanism of miR-182 in kidney fibrosis in polycystic kidney disease (PKD). Method We measured the expression of miR-182 in kidney tissue of autosomal dominant polycystic kidney disease (ADPKD). Additionally, we investigated the relationship between miR-182 and fibrotic protein by transfecting miR-182 mimics and miR-182 inhibitor into polycystic kidney cyst-lined epithelial cells, respectively. Furthermore, we observed the interaction between TGF-β1 and miR-182 and fibrinogen factors of cyst-lined epithelial cells after TGF-β1 intervention, and measured the expression of Smad2, 3 protein. Results (1) MiR-182 was positively correlated with fibrosis of cyst-lined epithelial cells; (2) TGF-β1 could induce fibrosis of cyst-lined epithelial cells; (3) the expression of miR-182 had an remarkably impact on the fibrosis induced by TGF-β1, but had little effect on the expression of TGF-β1; (4) the expression of Smad3 protein in TGF-β1 induce- cyst-lined epithelial cells were increased. Conclusion TGF-β and miR-182 promoting the fibrosis of polycystic kidney cyst -lined epithelial cells may be mediated by the TGF-β/Smad3 signaling pathway, of which Smad3 was an important regulator.

P0030MIR-182 INHIBITS KIDNEY FIBROSIS BY REGULATING TGF-Β1/SMAD3 PATHWAY IN ADPKD