Mouse strain-specific responses of mitochondrial respiratory function and cardiac hypertrophy to isoproterenol treatment.
- Author:
Shuang-Ling LI
1
;
Shun WANG
1
;
Yuan HE
1
;
Di ZHENG
1
;
Jian LYU
1
;
Ning-Ning GUO
1
;
Ying-Ying GUO
1
;
Li-Li LI
1
;
Ming-Xia FAN
2
;
Zhi-Hua WANG
1
Author Information
1. Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
2. Animal Center, Renmin Hospital of Wuhan University, Wuhan 430060, China. fanmingxia@whu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Animals;
Cardiomegaly/chemically induced*;
Heart Failure;
Isoproterenol/toxicity*;
Mice;
Mitochondria;
Myocytes, Cardiac/metabolism*
- From:
Acta Physiologica Sinica
2021;73(3):459-470
- CountryChina
- Language:English
-
Abstract:
Cardiac hypertrophy is a common pathological process of various cardiovascular diseases and eventually develops into heart failure. This paper was aimed to study the different pathological characteristics exhibited by different mouse strains after hypertrophy stimulation. Two mouse strains, A/J and FVB/nJ, were treated with isoproterenol (ISO) by osmotic pump to induce cardiac hypertrophy. Echocardiography was performed to monitor heart morphology and function. Mitochondria were isolated from hearts in each group, and oxidative phosphorylation function was assayed in vitro. The results showed that both strains showed a compensatory enhancement of heart contractile function after 1-week ISO treatment. The A/J mice, but not the FVB/nJ mice, developed significant cardiac hypertrophy after 3-week ISO treatment as evidenced by increases in left ventricular posterior wall thickness, heart weight/body weight ratio, cross sectional area of cardiomyocytes and cardiac hypertrophic markers. Interestingly, the heart from A/J mice contained higher mitochondrial DNA copy number compared with that from FVB/nJ mice. Functionally, the mitochondria from A/J mice displayed faster O
