Overexpression of microRNA-21-5p prevents the oxidative stress-induced apoptosis of RSC96 cells by suppressing autophagy.

AIM

We aim to study the anti-apoptotic effect of microRNA-21-5p (miR-21-5p) in the oxidative stress-induced apoptosis of Schwann cells and the relevant mechanism in this research, laying a foundation for the treatment of peripheral neuropathy (PNP).

METHODS AND MATERIALS

The oxidative stress model was established by using hydrogen peroxide (HO). ROS level were detected by DCFH-DA (2,7-Dichlorodi-hydrofluorescein diacetate). Western blot and fluorescence staining were used to detect the apoptosis and autophagy level. The miR-21-5p overexpression model was established by transfection of miR-21-5p mimics into RSC96 cells. Five groups of control group, HO group, HO + chloroquine (CQ) group, HO + miR-21-5p mimics group, and HO + miR-21-5p mimics+rapamycin (RAPA) group were included in our experiment.

KEY FINDINGS

Compared with control group, miR-21-5p was decreased in HO-treated RSC96 cells, while autophagy and apoptosis were both promoted. The result revealed that apoptosis was probably triggered by activation of autophagy in HO-treated group. In order to verify the relationship between autophagy and apoptosis more accurately, we used CQ to inhibit autophagy. Compared with HO-treated group, autophagy and apoptosis were both weakened in HO + CQ group. Subsequently, we found the antiapoptotic effect of miR-21-5p in this model, overexpression of miR-21-5p prevented cells from being damaged by oxidative stress, it induced the decrease of PTEN and the level of autophagy, leading to decreased level of apoptosis.

SIGNIFICANCE

The identified relationship between miR-21-5p, apoptosis, and autophagy promotes us to find a new mechanism to improve the treatment for PNP.