Study of senescence protein p66Shc on myocardial tissue repair in adult mice.
- Author:
Yuan ZHANG
1
;
Cheng-Zhen HUANG
2
;
Hou-Zao CHEN
2
;
Yu NIE
1
;
Miao-Qing HU
3
Author Information
1. National Health Commission Key Laboratory of Cardiovascular Regenerative Medicine, Fuwai Central China Cardiovascular Hospital, Central China Branch of National Center for Cardiovascular Diseases, Zhengzhou University, Zhengzhou 450046, China.
2. Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China.
3. State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing 100037, China. humiaoqing@fuwai.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Mice;
Body Weight;
Cicatrix/metabolism*;
Mice, Knockout;
Myocardial Infarction/genetics*;
Oxidative Stress;
Shc Signaling Adaptor Proteins/metabolism*;
Src Homology 2 Domain-Containing, Transforming Protein 1/metabolism*
- From:
Acta Physiologica Sinica
2023;75(6):946-952
- CountryChina
- Language:Chinese
-
Abstract:
Our previous study has shown that p66Shc plays an important role in the process of myocardial regeneration in newborn mice, and p66Shc deficiency leads to weakened myocardial regeneration in newborn mice. This study aims to explore the role of p66Shc protein in myocardial injury repair after myocardial infarction in adult mice, in order to provide a new target for the treatment of myocardial injury after myocardial infarction. Mouse myocardial infarction models of adult wild-type (WT) and p66Shc knockout (KO) were constructed by anterior descending branch ligation. The survival rate and heart-to-body weight ratio of two models were compared and analyzed. Masson's staining was used to identify scar area of injured myocardial tissue, and myocyte area was determined by wheat germ agglutinin (WGA) staining. TUNEL staining was used to detect the cardiomyocyte apoptosis. The protein expression of brain natriuretic peptide (BNP), a common marker of myocardial hypertrophy, was detected by Western blotting. The results showed that there was no significant difference in survival rate, myocardial scar area, myocyte apoptosis, and heart weight to body weight ratio between the WT and p66ShcKO mice after myocardial infarction surgery. Whereas the protein expression level of BNP in the p66ShcKO mice was significantly down-regulated compared with that in the WT mice. These results suggest that, unlike in neonatal mice, the deletion of p66Shc has no significant effect on myocardial injury repair after myocardial infarction in adult mice.
