Exercise Training Attenuates Age-induced Elevation in Bax/Bcl-2 Ratio, Apoptosis, and Remodeling in the Rat Heart.
From: Redox Biology and Cell Signaling Laboratory, Texas A&M University, College Station, Texas 77843-4243, USA.
The FASEB journal : official publication of the Federation of American Societies for Experimental Biology
- Publish Date: Apr 2006
- ISSN: 1530-6860
- Volume: 20
- Issue: 6
- Pages: 791-3
- Medium: Internet
- Language: English
- Citation (JAMA): Kwak Hyo-Bum, Song Wook, Lawler John M, et al. Exercise Training Attenuates Age-induced Elevation in Bax/Bcl-2 Ratio, Apoptosis, and Remodeling in the Rat Heart.. FASEB J. Apr 2006;20:791-3
Abstract
Aging is characterized by loss of myocytes, remodeling, and impaired contractile function in the heart. The rate of programmed cell death, or “apoptosis,” in the left ventricle increases with age, and contributes to a 30% reduction in myocytes. Aging may preferentially target the Bcl-2 pathway of apoptosis in the heart. Exercise can protect cardiac function of the aging heart, although the mechanisms are poorly understood. We tested the hypothesis that 12 wk of exercise training would attenuate age-induced increases in remodeling, apoptosis, and Bax/Bcl-2 ratio in rat left ventricle. We found that exercise training provided significant protection against loss of cardiac myocytes, reduction in number of myonuclei, reactive hypertrophy of remaining myocytes, and increased connective tissue in left ventricle of the aging rat heart. Exercise training significantly attenuated age-induced increases of apoptosis in the left ventricle, as indicated by lower DNA fragmentation, TUNEL-positive staining, and caspase-3 cleavage, when compared with left ventricles from the age-matched sedentary group. Further, exercise training in the aging reduced caspase-9 levels and Bax/Bcl-2 ratio by lowering Bax protein expression while increasing Bcl-2 levels. These are the first data to demonstrate protective effects of endurance exercise training against elevated apoptosis and remodeling in the aging heart.
Mesh Headings (Keywords): Aging, Animals, Apoptosis, Biological Markers, Caspases, Heart, Myocardium, Physical Conditioning, Animal, Proto-Oncogene Proteins c-bcl-2, Rats, Signal Transduction, Ventricular Remodeling, bcl-2-Associated X Protein
Check for Full Text / PubMed Unique Identifier (PMID): 16459353
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.