MicroRNA-205 inhibits the apoptosis of renal tubular epithelial cells via the PTEN/Akt pathway in renal ischemia-reperfusion injury.

Renal ischemia-reperfusion injury (IRI) is the main cause of acute kidney injury (AKI). Many studies on renal IRI have been performed recently, but effective treatments are still lacking. Evidence exists that small endogenous noncoding RNAs are involved in the ischemia-reperfusion process. This article aims to investigate whether microRNA-205 (miR-205) is involved in this process and to determine its role in the hypoxia-induced injury of renal tubular epithelial cells (TECs). We found that miR-205 was significantly downregulated in rats with renal IRI and in HK-2 cells with hypoxia-reoxygenation injury (HRI) in vitro. In vitro, overexpression of intracellular miR-205 by transfection of a miR-205 mimic significantly reduced apoptosis, and this antiapoptotic effect was antagonized by a miR-205 inhibitor. Moreover, we confirmed that PTEN is a target of miR-205. miR-205 exerted its protective effect by inhibiting HK-2 cell apoptosis and promoting HK-2 cell proliferation by inhibiting the expression of PTEN during HRI, and this protective effect was blocked by silencing PTEN. Therefore, we confirmed that miR-205 may target the PTEN/Akt signaling pathway to alleviate hypoxia-induced renal cell damage. miR-205 may be a new potential target for the treatment of renal IRI. AJTR