Correlation between Mic60 haploid insufficiency and cardiac aging in mouse
10.3760/cma.j.issn.0529-5807.2017.06.008
- VernacularTitle: 线粒体内膜蛋白Mic60半量缺失与小鼠心脏衰老的相关性
- Author:
Chunlou WANG
1
;
Lihong SUN
;
Yongsong YUE
;
Yamei NIU
;
Weimin TONG
Author Information
1. Department of Pathology, Institute of Basic Medical Sciences & School of Basic Medicine, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100005, China
- Publication Type:Journal Article
- Keywords:
Myocytes, cardiac;
Mitochondrial proteins;
Age factors;
Animal experimentation
- From:
Chinese Journal of Pathology
2017;46(6):406-410
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of Mic60 in cardiac aging.
Methods:Wild-type and Mic60+ /- male mice at age of 4-6 months (young group, n=6) and 18-20 months (aged group, n=9) were used. H&E and Masson staining of frozen and paraffin sections were subjected to morphologic evaluation of the cardiac tissue samples. SA-β-Gal staining was utilized to detect the activity of senescence-associated β-galactosidase. Western blot was performed to detect the expression of Mic60 and p21 in cardiac tissues.
Results:Expression of Mic60 in mouse cardiac tissue increased in an age-dependent manner. Haploid insufficiency of Mic60 resulted in an increased left ventricular wall thickness [(1.32±0.09) mm vs.(1.12±0.09) mm, P<0.05], cardiomyocyte hypertrophy[(474.9±27.6) μm2 vs.(358.8±48.7) μm2, P<0.05] and interstitial fibrosis [ (38.24±7.58) ×103μm2 vs.(25.81±4.12)×103μm2, P<0.05], increased activity of SA-β-Gal (2.26±0.24 vs.0.25±0.05, P<0.01) and higher expression of p21 (P<0.01) in aged mouse cardiac tissue, but not in young mice.
Conclusion:Haploid insufficiency of Mic60 leads to cardiac hypertrophy, interstitial fibrosis, increased activity of SA-β-Gal and higher expression of p21 in aged cardiac tissue in mice, suggesting that Mic60 may prevent cardiac aging.
