Preliminary Research for the Effect of EMRE on Myocardial Ischemia Injury in Experimental Mice
10.3969/j.issn.1000-3614.2017.07.019
- VernacularTitle:EMRE在小鼠心肌缺血损伤中的作用及其相关机制的研究
- Author:
Fengzhou LIU
;
Zhe JING
;
Mingli LIU
;
Enwei ZHANG
;
Jianghua NING
;
Jiao MOU
- Keywords:
Mitochondrial transporter proteins;
Myocardial ischemia
- From:
Chinese Circulation Journal
2017;32(7):701-706
- CountryChina
- Language:Chinese
-
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.
