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Oxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA ( Hotair ) was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of  Hotair  were exposed to I/R surgery. H9c2 cells were cultured and subjected to hypoxia/reoxygenation (H/R) stimulation to further verify the role and underlying mechanisms of  Hotair  in vitro. Histological examination, molecular detection, and functional parameters were determined in vivo and in vitro. In response to I/R or H/R treatment,  Hotair  expression was increased in a bromodomain-containing protein 4-dependent manner. Cardiac-restricted knockdown of  Hotair  exacerbated, whereas  Hotair  overexpression prevented I/R-induced oxidative stress, cardiac myocyte apoptosis, and cardiac dysfunction. Mechanistically, we observed that  Hotair  exerted its beneficial effects via activating AMP-activated protein kinase alpha (AMPK α ). Further detection revealed that  Hotair  activated AMPK α  through regulating the enhancer of zeste homolog 2/microRNA-451/calcium-binding protein 39 (EZH2/ miR-451 /Cab39) axis. We provide the evidence that endogenous lncRNA  Hotair  is an essential negative regulator for oxidative stress and cardiac myocyte apoptosis in myocardial I/R injury, which is dependent on AMPK α  activation via the EZH2/ miR-451 /Cab39 axis.

The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury