Acute exercise activates p38 MAPK and increases the expression of telomere protective genes in cardiac muscle.
Author: Ludlow AT1,2, Gratidao L1,3, Ludlow LW1,4, Spangenburg EE5, Roth SM1
Affiliation:
1Department of Kinesiology, School of Public Health, University of Maryland at College Park, College Park, MD, USA.
2Department of Cell Biology, The University of Texas Southwestern Medical Center, Dallas, Texas, USA.
3Kinesiology Graduate Program, Catholic University of Brasilia, Brazil.
4Department of Applied Physiology, Southern Methodist University, Dallas, Texas, USA.
5Department of Physiology, Brody School of Medicine, East Carolina Diabetes and Obesity Institute, East Carolina University, Greenville, NC, USA.
Conference/Journal: Exp Physiol.
Date published: 2017 Feb 6
Other:
Special Notes: doi: 10.1113/EP086189. [Epub ahead of print] , Word Count: 237
Age is the greatest risk factor for cardiovascular disease. Telomere length is shorter in the hearts of aged mice compared to young mice, and short telomere length has been associated with an increased risk of cardiovascular disease. One year of voluntary wheel running exercise attenuates the age-associated loss of telomere length and results in altered gene expression of telomere length maintaining and genome stabilizing proteins in heart tissue of mice. Understanding the early adaptive response of the heart to an endurance exercise bout is paramount to understanding the impact of endurance exercise on heart tissue and cells. To this end we studied mice before (BL), immediately post (TP1) and one-hour following (TP2) a treadmill running bout. We measured the changes in expression of telomere related genes (shelterin components), DNA damage sensing (p53, Chk2) and DNA repair genes (Ku70, Ku80), and MAPK signaling. TP1 animals had increased TRF1 and TRF2 protein and mRNA levels, greater expression of DNA repair and response genes (Chk2 and Ku80), and greater protein content of phosphorylated p38 MAPK compared to both BL and TP2 animals. These data provide insights into how physiological stressors remodel the heart tissue and how an early adaptive response mediated by exercise may be maintaining telomere length/stabilizing the heart genome through the up-regulation of telomere protective genes. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
PMID: 28166612 DOI: 10.1113/EP086189
BACK
