LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells

• Published in: Bioscience, biotechnology, and biochemistry Vol. 85; no. 4; pp. 866 - 873
• Main Authors: Lu, Ping, Xiao, Shihui, Chen, Shaoze, Fu, Youlin, Zhang, Peng, Yao, Yaner, Chen, Feng
• Format: Journal Article
• Language: English
• Published: England Oxford University Press 24.03.2021
• Subjects: RAGE; SNHG12; ischemia/reperfusion injury; hypoxia reoxygenation; H9c2 cells
• ISSN: 1347-6947; 1347-6947
• DOI: 10.1093/bbb/zbaa090

ABSTRACT Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. SNHG12 silencing enhanced the apoptosis of H/R-injured H9c2 cells, while SNHG12 overexpression relieved the cardiomyocyte apoptosis induced by H/R stimulation. Additionally, the suppression of SNHG12 significantly boosted the H/R-induced expression and the production of TNF-α, IL-6, and IL-1β, as well as the activation of NF-κB, which were fully reversed after overexpression of SNHG12. Mechanistically, SNHG12 adversely regulated the production of receptor for advanced glycation end products (RAGE) in H/R-stimulated H9c2 cells. Antibody blocking of RAGE alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have determined a valuable mechanism by which the high level of SNHG12 contributes to H9c2 cells against H/R injury through the reduction of RAGE expression. Graphical Abstract Graphical Abstract LncRNA SNHG12 induced by hypoxia reoxygenation suppresses the apoptosis of H9c2 cells through reducing expression of RAGE.