Abstract:

Ｏｂｊｅｃｔｉｖｅ：To illuminate the protective role of microRNA30s in AngⅡinduced podocyte injury.
Ｍｅｔｈｏｄｏｌｏｇｙ：(1) Mice were infused with AngⅡ at a dose of 1 000 ng/kg/min for 28 days with the osmotic minipumps implanted subcutaneously. The expression of miR30s in mice glomeruli was examined by qRTPCR and in situ hybrization. The expressions of TRPC6, PPP3CA、 PPP3CB、 PPP3R1 and NFATC3 were tested by western blotting and immunohistochemical. (2) To examine the protective effects of miR30s in AngⅡtreated mice, miR30aexpressing lentivirus or control lentivirus was injected via the tail vein on day 14 during the AngⅡ infusion. The glomerular podocyte damage was evaluated with proteinuria，PAS staining and podocyte apoptosis and foot process effacement were used to measure podocye injury.(3) treated miR30overexpressed podocyte with 10-6 mol/L AngⅡ, and cytoskeletal injury and cell apoptosis were examined by Factin staing and Annexin Vflow cytometry.
Ｒｅｓｕｌｔｓ：(1) Ang II infusion induced the downregulation of miR30 family and the activation of calcium/calcineurin signaling；（2）miR30a could inhibit AngⅡinduced activation of calcium/calcineurin signaling and then relieve AngⅡinduced podocyte injury；(3) Exogenous miR30a protected podocytes from AngⅡinduced cytoskeletal damage and apoptosis in vitro. 
Ｃｏｎｃｌｕｓｉｏｎ：miR30s could protect podocyte from AngⅡinduced damage likely through calcium/calcineurin signaling inhibition.