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Am J Physiol Regul Integr Comp Physiol 295: R1623-R1630, 2008. First published September 10, 2008; doi:10.1152/ajpregu.00089.2008
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EXERCISE AND RESPIRATORY PHYSIOLOGY

Exercise promotes {alpha}7 integrin gene transcription and protection of skeletal muscle

Marni D. Boppart,1,2 Sonja E. Volker,3 Nicole Alexander,1,2 Dean J. Burkin,4 and Stephen J. Kaufman3

1Department of Kinesiology and Community Health, 2Beckman Institute for Advanced Science and Technology, and 3Department of Cell and Developmental Biology, University of Illinois, Urbana, Illinois; 4Department of Pharmacology, University of Nevada, Reno, Nevada

Submitted 7 February 2008 ; accepted in final form 1 September 2008

The {alpha}7β1 integrin is increased in skeletal muscle in response to injury-producing exercise, and transgenic overexpression of this integrin in mice protects against exercise-induced muscle damage. The present study investigates whether the increase in the {alpha}7β1 integrin observed in wild-type mice in response to exercise is due to transcriptional regulation and examines whether mobilization of the integrin at the myotendinous junction (MTJ) is a key determinant in its protection against damage. A single bout of downhill running exercise selectively increased transcription of the {alpha}7 integrin gene in 5-wk-old wild-type mice 3 h postexercise, and an increased {alpha}7 chain was detected in muscle sarcolemma adjacent to tendinous tissue immediately following exercise. The {alpha}7B, but not {alpha}7A isoform, was found concentrated and colocalized with tenascin-C in muscle fibers lining the MTJ. To further validate the importance of the integrin in the protection against muscle damage following exercise, muscle injury was quantified in {alpha}7–/– mice. Muscle damage was extensive in {alpha}7–/– mice in response to both a single and repeated bouts of exercise and was largely restricted to areas of high MTJ concentration and high mechanical force near the Achilles tendon. These results suggest that exercise-induced muscle injury selectively increases transcription of the {alpha}7 integrin gene and promotes a rapid change in the {alpha}7β integrin at the MTJ. These combined molecular and cellular alterations are likely responsible for integrin-mediated attenuation of exercise-induced muscle damage.

exercise; injury; repeated bout effect; tenascin-C



Address for reprint requests and other correspondence: S. J. Kaufman, Dept. of Cell and Developmental Biology, B107 Chemical and Life Sciences Laboratory, 601 South Goodwin Ave., Urbana, IL 61801 (e-mail: stephenk{at}illinois.edu)







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