EPHB2 knockdown mitigated MI-induced myocardial injury by inhibiting MAPK signaling

Abstract

Myocardial infarction (MI) is a common disease in the cardiovascular field. The incidence of ventricular remodeling dysplasia and heart failure increases significantly after MI. The objective of this study was to investigate whether EPHB2 could regulate myocardial injury after MI and explore its regulatory pathways. RT-qPCR and Western blot were used to verify the expression of EPHB2 in MI mice, and then shRNA knockdown of EPHB2 was used to confirm the relationship between EPHB2 expression and disease progression. The levels of inflammation, apoptosis and fibrosis were detected by tissue staining. Related factors were detected by RT-qPCR, Western blot or ELISA. Further, the signaling pathway through which EPHB affected MI processes was detected and preliminarily confirmed by Western blot. EPHB2 was significantly overexpressed in heart tissue of MI mice. Knockdown of EPHB2 gene significantly downregulated immune factors and apoptotic factors, and alleviated mi-induced cardiac tissue damage and functional decline in mice. The MAPK pathway was found to be a downstream pathway in which EPHB2 acted. Knockdown EPHB2 down-regulates phosphorylation of MAPK pathway-related proteins. In mouse models, knockdown EPHB2 alleviated MI-induced cardiac function decline, inflammation and apoptosis of myocardial tissue, and myocardial fibrosis. This process may be achieved through the MAPK pathway.