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Protection of MICU1 against myocardial hypertrophy induced by angiotensin Ⅱ
- Source :
- Medical Journal of Chinese People's Liberation Army, Vol 42, Iss 12, Pp 1051-1055 (2017)
- Publication Year :
- 2017
- Publisher :
- Editorial Board of Medical Journal of Chinese People's Liberation Army, 2017.
-
Abstract
- Objective To investigate the role of mitochondrial calcium uptake 1 (MICU1) in myocardial hypertrophy of mice and underlying mechanism. Methods The model of myocardial hypertrophy was established via incubation of mouse cardiac myocytes (MCM) with 300nmol/L angiotensin Ⅱ (Ang Ⅱ) for 48 hours in vitro. After that, MICU1 specific small interfering RNA (siRNA) was delivered to knockdown MICU1 levels in MCM. On the other hand, adenovirus-mediated over-expression of MICU1 was transfected into MCM. Accordingly, the expressions of ANP and BNP in myocardial cells were measured by qRT- PCR. Mitochondrial membrane potential and ATP contents were detected by JC-1 assay kit and ATP assay kit, respectively. Then, Western blotting and qRT-PCR were used to detect the levels of MICU1 in myocardial cells. The mitochondrial Ca2+ contents were measured via atomic absorption flame spectroscopy. The size of myocardial cells was determined by α-actinin staining. Results Mitochondrial membrane potential and ATP contents in hypertrophic cardiomyocytes induced by AngⅡ were both decreased. Meanwhile, myocardial hypertrophy significantly increased mitochondrial Ca2+ contents but decreased MICU1 levels. With the method of genetic intervention, we found that MICU1 deficiency exacerbated mitochondrial Ca2+ overload, increased cell surface and elevated the expression of BNP. Conversely, the overexpression of MICU1 obviously decreased mitochondrial Ca2+ overload, cell surface of MCM and expressions of ANP and BNP. Conclusion MICU1 alleviates AngⅡ-induced myocardial hypertrophy via inhibiting mitochondrial Ca2+ overload. DOI: 10.11855/j.issn.0577-7402.2017.12.05
Details
- Language :
- Chinese
- ISSN :
- 05777402
- Volume :
- 42
- Issue :
- 12
- Database :
- OpenAIRE
- Journal :
- Medical Journal of Chinese People's Liberation Army
- Accession number :
- edsair.doajarticles..6e29edd4a2c84540830d4138e8b84a3d