Exertional heat stroke causes long-term skeletal muscle epigenetic reprogramming, altered gene expression, and impaired satellite cell function in mice

Author:

Murray Kevin O.1ORCID,Brant Jason O.23ORCID,Spradlin Ray A.1,Thome Trace1ORCID,Laitano Orlando1ORCID,Ryan Terence E.1ORCID,Riva Alberto34,Kladde Michael P.53ORCID,Clanton Thomas L.1ORCID

Affiliation:

1. Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, Florida, United States

2. Department of Biostatistics, University of Florida, Gainesville, Florida, United States

3. University of Florida Health Cancer Center, University of Florida, Gainesville, Florida, United States

4. Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, Florida, United States

5. Department of Biochemistry and Molecular Biology, College of Medicine, University of Florida, Gainesville, Florida, United States

Abstract

Exertional heat stroke (EHS) in mice induces long-term molecular and functional changes in limb muscle that could reflect a loss of “resilience” to further stress. The phenotype was characterized by altered caffeine sensitivity and suppressed satellite cell proliferative potential. This was accompanied by changes in gene expression and DNA methylation consistent with ongoing muscle remodeling and stress adaptation. We propose that EHS may induce a prolonged vulnerability of skeletal muscle to further stress or injury.

Funder

American Heart Association

Bankhead-Coley Foundation

DOD | Military Health System

HHS | National Institutes of Health

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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