ABSTRACT
[This corrects the article DOI: 10.1016/j.heliyon.2023.e17388.].
ABSTRACT
Purpose: The aim of this study was to investigate the protective effect of long non-coding lnc-PXMP4-2-4 on myocardial cell damage caused by acute myocardial infarction (AMI). Methods: Peripheral blood mononuclear cells (PBMC) were collected from 24 patients with AMI on the day of admission, the first day after percutaneous coronary intervention (PCI) and the third day after surgery, and 24 patients with clinical control group. Real-time quantitative PCR(QRT-PCR) was used to detect the expression of related genes. Then in human cardiomyocytes (AC16), Cell Counting Kit-8 (CCK-8) was used to determine cell viability, lactate dehydrogenase release assay (LDH) was used to determine the release of lactate dehydrogenase, PCR was used to detect the expression of genes, cell death was detected by flow cytometry, and the expression of related proteins was measured by Western blot. The effect of lnc-PXMP4-2-4 was further studied by silencing and overexpressing lnc-PXMP4-2-4. Results: Compared with clinical control group, the expression of lnc-PXMP4-2-4 in PBMC of AMI patients was significantly higher than it. Compared with pre-operation, the expression of lnc-PXMP4-2-4 was significantly up-regulated on day 1 after PCI, and recovered to pre-operation level on day 3 after surgery. In AC16 cells, lnc-PXMP4-2-4 inhibited the proliferation of AC16, promoted the release of LDH and increased cell death, aggravated the cardiomyocyte injury caused by H2O2, and inhibited the expression of JAK2 and STAT3 mRNA and protein. The up-regulation of lnc-PXMP-4-2-4 had the opposite effect. In addition, the inhibition of the signal pathway by JAK2/STAT3 pathway inhibitor AG490 partially weakened the enhanced viability of AC16 cells, decreased LDH release and apoptosis induced by lnc-PXMP4-2-4 overexpression, increased Bcl-2 expression and down-regulated Bax expression. Conclusion: Therefore, we conclude that lnc-PXMP4-2-4 protects cardiomyocytes from injury by activating the JAK2/STAT3 signaling pathway.
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.