Regulatory roles of miR-22/Redd1-mediated mitochondrial ROS and cellular autophagy in ionizing radiation-induced BMSC injury.

ABSTRACT: Ionizing radiation (IR) response has been extensively investigated in BMSCs with an increasing consensus that this type of cells showed relative radiosensitivity in vitro analysis. However, the underlying mechanism of IR-induced injury of BMSCs has not been elucidated. In current study, the regulatory role of miR-22/Redd1 pathway-mediated mitochondrial reactive oxygen species (ROS) and cellular autophagy in IR-induced apoptosis of BMSCs was determined. IR facilitated the generation and accumulation of mitochondrial ROS, which promoted IR-induced apoptosis in BMSCs; meanwhile, cellular autophagy activated by IR hold a prohibitive role on the apoptosis program. The expression of miR-22 significantly increased in BMSCs after IR exposure within 24 h. Overexpression of miR-22 evidently accelera

SUBMITTER: Liu Z 

PROVIDER: S-EPMC6405932 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature