Effects of different intensity exercise training on apoptosis-related microRNAs and the targeted proteins in cardiomyocytes.
10.12047/j.cjap.5502.2018.023
- Author:
Yong-Cai ZHAO
1
;
Jin-Mei FU
2
;
Bing-Hong GAO
1
Author Information
1. Shanghai University of Sport, Shanghai 200438.
2. Institute for Sports Science of Jiangxi Province, Nanchang 330006, China.
- Publication Type:Journal Article
- Keywords:
apoptosis;
cardiomyocyte;
exercise;
mice;
microRNAs
- MeSH:
Animals;
Apoptosis;
Apoptosis Regulatory Proteins;
metabolism;
Male;
Mice;
Mice, Inbred C57BL;
MicroRNAs;
metabolism;
Myocardium;
metabolism;
pathology;
Myocytes, Cardiac;
cytology;
metabolism;
Physical Conditioning, Animal;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
RNA-Binding Proteins;
metabolism;
Random Allocation
- From:
Chinese Journal of Applied Physiology
2018;34(1):93-96
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To detect the levels of miR-1, miR-21 and their targeted proteins in hearts of mice after different exercise training, and discuss potential molecular mechanism.
METHODS:Male C57BL/6 mice were randomly divided to 3 groups:sedentary (SE), exercise training 1(ET1) and exercise training 2 (ET2). SE did not do any exercise; ET1 undertook swimming training for 8 weeks, once a day, 5 days/week. Swimming 30 min in the 1 week, and the duration was increased 10 min per week to 90 min and maintained in the 7 and 8 week. ET2 performed the same work as ET1 and switched to twice a day by the end of the 5th week. TUNEL assay was applied to test myocardial apoptosis. Western blot and RT-PCR were used to detect proteins and miRs levels respectively.
RESULTS:Compared with SE, in ET1, myocardial apoptosis and miR-1 level did not change, but its targeted protein Bcl-2 increased significantly(<0.01). miR-21 and its targeted protein PDCD4 did not change significantly. In ET2, myocardial apoptosis and miR-1 level were decreased significantly(<0.05). Bcl-2 was increased significantly(<0.01). miR-21 also increased significantly (<0.05), but PDCD4 did not decrease significantly.
CONCLUSIONS:Exercise training in ET2 other than ET1 could down-regulate myocardial apoptosis. Alterations of miR-1 and Bcl-2 may be responsible for this cardioprotection. PDCD4 is not sensitive to exercise training, it is likely that miR-21 and other targeted proteins participate in exercise-regulative apoptosis.
