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

Guiju Feng; Hong Zhang; Qingling Guo; Xin Shen; Shouyan Wang; Yi Guo; Xia Zhong

doi:10.1016/j.heliyon.2023.e17388

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

Heliyon. 2023 Jun 21;9(6):e17388. doi: 10.1016/j.heliyon.2023.e17388. eCollection 2023 Jun.

Authors

Guiju Feng¹, Hong Zhang¹, Qingling Guo², Xin Shen¹, Shouyan Wang¹, Yi Guo¹, Xia Zhong¹

Affiliations

¹ Department of General Practice, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China.
² Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 250021, China.

Abstract

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.

Keywords: Acute myocardial infarction; NONHSAT098487.2; Notch signalling pathway; Oxidative stress injury; lncRNA.