Long noncoding RNA HOTAIR regulates autophagy via the miR-20b-5p/ATG7 axis in hepatic ischemia/reperfusion injury.

Hepatic ischemia/reperfusion (I/R) injury is a pathological process that induces oxidative stress, hepatocyte apoptosis, autophagy, and increased inflammatory cytokines. The process can result in liver injury and dysfunction. Long noncoding RNAs (lncRNAs) are associated with the process of I/R; however, the underlying mechanism is not clear. The present study aimed to investigate the regulatory effect of lncRNA HOTAIR on autophagy during hepatic I/R injury. The expression levels of HOTAIR, LC3, and ATG7 were examined in a hepatic I/R model. We found that HOTAIR and ATG7 expression levels were upregulated and the autophagy level was significantly increased during I/R liver injury. In isolated hepatocytes, knockdown of the expression of HOTAIR attenuated autophagy induced by hydrogen peroxide. Using the bioinformatics database of TargetScan and starbase, we predicted microRNA miRNA-20b-5p might participate in the regulation between HOTAIR and ATG7. The miR-20b-5p level was significantly decreased in I/R livers and was identified to target ATG7 and inhibit its expression. In addition, HOTAIR can function as competing endogenous RNA for miR-20b-5p and attenuates its inhibitory effect on ATG7. Taken together, our findings revealed that HOTAIR regulates autophagy via the miR-20b-5p/ATG7 axis in hepatic I/R injury, which may serve as basis to develop novel therapeutic strategies to treat hepatic I/R injury.