NEAT1 promotes myocardial ischemia-reperfusion injury via activating the MAPK signaling pathway

Myocardial ischemia-reperfusion (IR) injury is a common cardiovascular problem, which remains a major cause of death in the world. Emerging evidence has suggested that long noncoding RNAs are crucial players in myocardial injury. However, the functional involvement of nuclear enriched abundant transcript 1 (NEAT1) in myocardial IR injury remains poorly investigated. Our study focused on the mechanism of NEAT1 in myocardial IR injury. Here, we reported a crucial role for NEAT1 in exacerbating cardiac IR injury. NEAT1 was greatly increased in myocardial IR injury mice models. As exhibited knockdown of NEAT1 resulted in attenuated myocardial IR injury in vivo. In addition, we found that NEAT1 was dramatically induced by hypoxia/reoxygenation in H9c2 cells. Lactate dehydrogenase (LDH), malondialdehyde, reactive oxygen species levels, and endoplasmic reticulum stress-regulated cardiomyocyte apoptosis were inhibited by the downregulation of NEAT1. Here, it was shown that knockdown of NEAT1 was able to repress tumor necrosis factor-alpha, interleukin-1 beta, and IL-6 expression. The silence of NEAT1 protected against IR injury via decreasing troponin levels, cardiocytes apoptosis, creatine kinase, and lactate LDH release in vivo. Meanwhile, the mitogen-activated protein kinase (MAPK) signaling was involved in NEAT1-mediated myocardial IR injury. In summary, our data indicated that NEAT1 contributed to myocardial IR injury via activating the MAPK pathway.