MicroRNA-29b protected renal fibrosis

It has been demonstrated that the Angiotensin II (Ang II) contents and its receptor density in the kidney of young spontaneously hypertensive rats (SHRs) were significantly higher than in age-matched Wistar-Kyoto rats (WKYs). Ang II has been proved to induce Epithelial-Mesenchymal Transition (EMT). The present study was aimed at testing the role of miRNA-29b (miR-29b) in Ang II-induced EMT. Differential expression of miR-29b in renal cortex between 15-weeks SHRs and age-matched WKYs was determined by real-time quantitative polymerase chain reaction (RT-qPCR). The effect of miR-29b on EMT-associated genes such as transforming growth factor (TGF-b), a-smooth muscle actin (aSMA), CollagenI (ColI) was examined after transfecting miR-29b mimics (24 h before treatment with 10M Ang II) and miR-29b inhibitor into cultured renal tubular epithelial cells line_NRK-52E cells. Analysis of these genes expression was confirmed by RT-qPCR, western blot and immunofluorescence staining. Downregulation of miR-29b in renal cortex of SHRs was demonstrated by RT-qPCR compared with that of WKYs. Transfection of miR-29b inhibitor significantly increased the expression of TGF-b, a-SMA and ColI, while transfection of miR-29b mimics inhibited Ang II-induced upregulation of these genes expression. Expression of miR-29b in renal cortex of SHRs was decreased. The miR-29b may play a crucial role in EMT. Downregulation of miR-29b may exert a similar effect on NRK-52E cells as those seen in treatment of Ang II, while upregulation of miR-29b may protect NRK-52E cells from EMT induced by Ang II.