ABSTRACT
To study the effect of essential MCU regulator (EMRE) on myocardial ischemia injury in experimental mice with underlining mechanism. Methods: Myocardial EMRE expression was up-regulated by EMRE adenovirus (Ad-EMRE) injection in mice myocardium tissue. Our research included in 3 groups: Sham operation group, sham mice received myocardium injection of eGFP adenovirus (Ad-eGFP); Myocardial infarction (MI) control group, the mice received Ad-eGFP injection and 48 hours later had coronary LAD ligation to establish MI model; MI treatment group, MI mice received Ad-EMRE injection. All animals were treated in 3 weeks. Mice cardiac function was examined by ultrasound; cardiomyocyte hypertrophy was evaluated by wheat germ agglutinin (WGA) staining, collagen fibrosis was measured by Masson staining, cell apoptosis was determined by TUNEL assay, protein expressions of EMRE, caspase-3 and caspase-9 were detected by Western blot analysis and mitochondrial reactive oxygen species (ROS) was assayed by MitoSOX fluorescence probe. Results: Compared with MI control group, MI treatment group showed the worse cardiac function, aggravated cardiac hypertrophy and elevated collagen fibrosis; in addition, MI treatment group had obviously increased cardiomyocyte apoptosis and increased protein expressions of Caspase-3, Caspase-9 and more mitochondrial ROS production. Conclusion: Over expressed EMRE can increase mitochondrial ROS production, induce cardiomyocyte apoptosis and therefore, aggravate myocardial ischemia injury in experimental mice.