Down-regulation of IncRNA KCNQ10T1 protects against myocardial ischemia/reperfusion injury following acute myocardial infarction

This study aimed to investigate the protective effects of long non-coding RNA KCNQ10T1 against myocardial ischemia/reperfusion (I/R) injury following acute myocardial infarction, as well as its regulatory mechanism. We used the cardiac muscle H9c2 cells under condition of oxygen glucose deprivation followed by reperfusion (OGD/R) to induce myocardial I/R injury. Then H9C2 cells were transfected with si-NC, si-KCNQ10T1, pc-NC, pc-KCNQ10T1, si-AdipoRl and si-AdipoR2, respectively. The myocardial cell viability and apoptosis were respectively detected. In addition, the expression levels of inflammatory factors, apoptosis-related proteins and p38 MAPK/NF-kappa B pathway-related proteins were detected. Besides, an inhibitor of p38 MAPK/NF-kappa B pathway SB203580 was used to treat cells to verify the relationship between KCNQ10T1 and p38 MAPK/NF-kappa B pathway. The expression of KCNQ10T1 was significantly up-regulated in OGD/R-induced myocardial H9C2 cells. The OGD/R-induced decreased cell viability and AdipoRl expression could be reversed after suppression of KCNQ10T1. In addition, suppression of KCNQ10T1 reduced OGD/R-induced increased expressions of TNF-alpha, IL-6 and IL-1 beta and OGD/R-induced increased cell apoptosis, which were reversed after knockdown of AdipoRi. Besides, suppression of KCNQ10T1 significantly down-regulated the OGD/R-induced increased expression of p-p38 and p-NF-kappa B, which were also reversed after knockdown of AdipoRi. Moreover, SB203580, an inhibitor of p38 MAPK/NF-kappa B signal pathway, could further enhance the inhibitory effects of KCNQ10T1 suppression on the expression of p-p38, TNF-a, IL-6, IL-1 beta and p-NF-kappa B in OGD/R-induced myocardial H9C2 cells. Suppression of KCNQ10T1 may prevent myocardial I/R injury following acute myocardial infarction via regulating AdipoRl and involving in p38 MAPK/NF-kappa B signal pathway. (C) 2017 Elsevier Inc. All rights reserved.