NONHSAT098487.2 protects cardiomyocytes from oxidative stress injury by regulating the Notch pathway

• Published in: Heliyon Vol. 9; no. 6; p. e17388
• Main Authors: Feng, Guiju, Zhang, Hong, Guo, Qingling, Shen, Xin, Wang, Shouyan, Guo, Yi, Zhong, Xia
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.06.2023; Elsevier
• Subjects: Acute myocardial infarction; lncRNA; NONHSAT098487.2; Notch signalling pathway; Oxidative stress injury; Notch signalling pathway; lncRNA; NONHSAT098487.2; Acute myocardial infarction; Oxidative stress injury
• ISSN: 2405-8440; 2405-8440
• DOI: 10.1016/j.heliyon.2023.e17388

Acute myocardial infarction has increasingly become a global health problem and is a primary cause of cardiovascular disease-related death. Although long noncoding RNAs have been reported to play an important role in various cardiovascular diseases, their protective effects on cardiomyocytes against reactive oxygen species-induced oxidative injury have nonetheless been poorly studied. The present study aims to explore the effect of a novel long noncoding RNA, NONHSAT098487.2, on cardiomyocyte injury induced by H2O2. The expression of NONHSAT098487.2 and pathway-related genes was evaluated by quantitative real-time polymerase chain reaction. Cell viability, release of lactate dehydrogenase, and apoptosis levels were detected by cell counting kit-8, lactate dehydrogenase release assay, and flow cytometry analysis, respectively. The protein levels were estimated by western blotting. The results showed that NONHSAT098487.2 was expressed at a high level in peripheral blood mononuclear cells from acute myocardial infarction patients, which showed a positive correlation with the HS-TnT and CK-MB levels of patients. Furthermore, it is also upregulated in human AC16 cardiomyocytes treated with H2O2 or exposed to hypoxia/reoxygenation conditions. Knockdown of NONHSAT098487.2 restrained the Notch signalling pathway and aggravated H2O2-induced cardiomyocyte oxidative stress injury. In contrast, overexpression of NONHSAT098487.2 activated the Notch signalling pathway and suppressed H2O2-induced oxidative stress injury. However, the Notch inhibitor DAPT weakened the protective effects of NONHSAT098487.2. Therefore, the novel lncRNA NONHSAT098487.2 may play a role in protecting cardiomyocytes from oxidative stress injury by regulating the Notch pathway.