Preliminary Research for the Effect of EMRE on Myocardial Ischemia Injury in Experimental Mice / 中国循环杂志
Chinese Circulation Journal
; (12): 701-706, 2017.
Article
em Zh
| WPRIM
| ID: wpr-617049
Biblioteca responsável:
WPRO
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.
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Base de dados:
WPRIM
Idioma:
Zh
Revista:
Chinese Circulation Journal
Ano de publicação:
2017
Tipo de documento:
Article