LncRNA EBLN3P inhibits myocardial inflammation and apoptosis after acute myocardial infarction via targeting miR-675-3p

Abstract

Abstract Objectives Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of the coronary arteries. This study aimed to investigate the potential mechanisms of lncRNA EBLN3P in the development of AMI. Methods This study recruited 109 patients with AMI and 117 healthy controls. The hypoxia/reoxygenation (H/R) cell model was primarily utilized to simulate in vivo ischemia-reperfusion injury of tissues and organs. The expression levels of EBLN3P were assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The concentrations of TNF-α, IL-6, and IL-1β were quantified via enzyme-linked immunosorbent assay (ELISA). Apoptosis was evaluated using flow cytometry. Additionally, the dual-luciferase reporter assay was utilized to confirm the targeting relationship between EBLN3P and miR-675-3p. Results EBLN3P was significantly downregulated in the serum of AMI patients. The receiver operating characteristic (ROC) curve analysis demonstrated that EBLN3P exhibited high diagnostic accuracy for AMI. Hypoxia/reoxygenation (H/R) treatment led to a marked decrease in EBLN3P expression levels, which could be significantly restored by transfecting EBLN3P post H/R treatment. H/R treatment significantly elevated the levels of TNF-α, IL-1β, and IL-6, but EBLN3P transfection partially reversed this effect. Additionally, H/R treatment resulted in a significant increase in the apoptosis rate, which EBLN3P transfection markedly reduced following H/R. EBLN3P targeted and regulated miR-675-3p, with their expression levels being negatively correlated. Furthermore, under H/R conditions, co-expression of EBLN3P and miR-mimic partially alleviated the effects of EBLN3P on cell behavior. Conclusions EBLN3P was involved in the regulatory mechanism of AMI by targeting miR-675-3p.