MiR‐27a‐5p regulates apoptosis of liver ischemia‐reperfusion injury in mice by targeting Bach1

Abstract Ischemia‐reperfusion (I/R) injury causes cellular dysfunction and a series of immune or apoptotic reactions. Bach1 is a mammalian transcription factor that represses Hmox1, which encodes heme oxygenase‐1 (HO‐1) that can degrade heme into free iron, carbon monoxide, and biliverdin, to play an important role in antioxidant, anti‐inflammatory, and antiapoptotic activities. MicroRNAs (miRNAs) can be found in a variety of eukaryotic cells and viruses, a class of noncoding small RNAs that are encoded by endogenous genes. The aims of this study were to determine whether miR‐27a‐5p targets Bach1 and regulates cellular death; the dual‐luciferase reporter assay was used to detect this and the results showed that miR‐27a‐5p significantly decreased the luciferase activity of the Bach1 3′‐untranslated region. MiR‐27a‐5p was increased in mice during hepatic I/R and Bach1 was decreased. By transfecting the AML12 cells with the mimic, inhibitor miR‐27a‐5p in hypoxia/reoxygenation (H/R) models showed that overexpression of miR‐27a‐5p decreased Bach1 messenger RNA, upregulated HO‐1 expression, and promoted antiapoptotic Bcl‐2 and downregulated proapoptotic caspase‐3 gene expression. In contrast, the miR‐27a‐5p inhibitor yielded the opposite results. Meanwhile, transfection with Bach1 small interference RNA obviously upregulated the protein levels of HO‐1 and resulted in an increase in Bcl‐2 and a decrease in caspase‐3 protein levels. Thus, we can conclude that miR‐27a‐5p is relevant to liver I/R injury and overexpression of miR‐27a‐5p may alleviate apoptosis in H/R injury by targeting Bach1 in vitro.