The Serum of MEF2D Expression in Patients with Myocardial Infarction, May be Clinical Indicators and it Mediated ROS Signaling by HDAC5

Abstract Objectives: In this study, we explain that the function of MEF2D gene in myocardial infarction and its possible mechanism. Methods: Patients with MI and normal volunteers were collected. The left anterior descending arteries (LAD) of mice were ligated to induce myocardial infarction. H9c2 cells were stimulated with 5% oxygen (O2) and 5% carbon dioxide (CO2) and 90% N2 for 24 h. Quantitative polymerase chain reaction (qPCR), Microarray experiments, Western blot, Enzyme-linked immunosorbent assay (ELISA) and Immunofluorescent staining were used at this experiment. Results: MEF2D mRNA and protein expressions in heart tissue of patients and mice with myocardial infarction were reduced. MEF2D protein prevented Myocardial infarction in mice of myocardial infarction. The inhibition of MEF2D aggravated Myocardial infarction in mice of myocardial infarction. MEF2D gene promoted ROS-induced oxidative stress in vitro model of myocardial infarction. MEF2D interlinkage HDAC5 to reduced oxidative stress in vivo model or vitro model. The regulation of HDAC5 adjusted the function of MEF2D in vitro model. Discussion: These data confirmed that the serum of MEF2D expression in patients with Myocardial infarction was reduced, may be clinical indicators and it inhibited ROS-induced oxidative stress signaling by HDAC5. Thus, our results suggest that targeting MEF2D may provide an approach for the treatment of myocardial infarction.