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1 School of Kinesiology, University of Illinois Chicago, Chicago, IL, USA
2 Global Research and Development, Pfizer, Groton, CT, USA
* To whom correspondence should be addressed. E-mail: thornb1{at}bioeng.ucsd.edu.
The capacity for skeletal muscle to recover its mass following periods of unloading (regrowth) has been reported to decline with age. Although the mechanisms responsible for the impaired regrowth are not known, it has been suggested that aged muscles have a diminished capacity to sense and subsequently respond to a given amount of mechanical stimuli (mechanosensitivity). To test this hypothesis, EDL muscles from young (2-3 month) and old (26-27 month) mice were subjected to intermittent 15% passive stretch (ex vivo) as a source of mechanical stimulation and analyzed for alterations in the phosphorylation of stress activated protein kinase (p38), ribosomal S6 kinase (p70S6k) and the p54 jun-N-terminal-kinase (JNK2). The results indicated that the average magnitude of specific tension (mechanical stimuli) induced by 15% stretch was similar in muscles from young and old mice. Young and old muscles also revealed similar increases in the magnitude of mechanically-induced p38, p70S6k (threonine/serine 421/424 and threonine 389) and JNK2 phosphorylation. In addition, co-incubation experiments demonstrated that the release of locally acting growth factors was not sufficient for the induction of JNK2 phosphorylation, suggesting that JNK2 was activated by a mechanical rather than a mechanical/growth factor-dependent mechanism. Taken together, the results of this study demonstrate that aging does not alter the mechanosensitivity of the p38, p70S6k and JNK2 signaling pathways in skeletal muscle.
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