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Alterations in the muscle force transfer apparatus in aged rats during unloading and reloading: impact of microRNA‐31


Journal article


David C. Hughes, George R. Marcotte, Leslie M. Baehr, Daniel W D West, A. Marshall, Scott M. Ebert, A. Davidyan, C. Adams, S. Bodine, K. Baar
Journal of Physiology, 2018

Semantic Scholar DOI PubMed
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APA   Click to copy
Hughes, D. C., Marcotte, G. R., Baehr, L. M., West, D. W. D., Marshall, A., Ebert, S. M., … Baar, K. (2018). Alterations in the muscle force transfer apparatus in aged rats during unloading and reloading: impact of microRNA‐31. Journal of Physiology.


Chicago/Turabian   Click to copy
Hughes, David C., George R. Marcotte, Leslie M. Baehr, Daniel W D West, A. Marshall, Scott M. Ebert, A. Davidyan, C. Adams, S. Bodine, and K. Baar. “Alterations in the Muscle Force Transfer Apparatus in Aged Rats during Unloading and Reloading: Impact of MicroRNA‐31.” Journal of Physiology (2018).


MLA   Click to copy
Hughes, David C., et al. “Alterations in the Muscle Force Transfer Apparatus in Aged Rats during Unloading and Reloading: Impact of MicroRNA‐31.” Journal of Physiology, 2018.


BibTeX   Click to copy

@article{david2018a,
  title = {Alterations in the muscle force transfer apparatus in aged rats during unloading and reloading: impact of microRNA‐31},
  year = {2018},
  journal = {Journal of Physiology},
  author = {Hughes, David C. and Marcotte, George R. and Baehr, Leslie M. and West, Daniel W D and Marshall, A. and Ebert, Scott M. and Davidyan, A. and Adams, C. and Bodine, S. and Baar, K.}
}

Abstract

Force transfer is integral for maintaining skeletal muscle structure and function. One important component is dystrophin. There is limited understanding of how force transfer is impacted by age and loading. Here, we investigate the force transfer apparatus in muscles of adult and old rats exposed to periods of disuse and reloading. Our results demonstrate an increase in dystrophin protein during the reloading phase in the adult tibialis anterior muscle that is delayed in the old muscle. The consequence of this delay is an increased susceptibility towards contraction‐induced muscle injury. Central to the lack of dystrophin protein is an increase in miR‐31, a microRNA that inhibits dystrophin translation. In vivo electroporation with a miR‐31 sponge led to increased dystrophin protein and decreased contraction‐induced muscle injury in old skeletal muscle. Overall, our results detail the importance of the force transfer apparatus and provide new mechanisms for contraction‐induced injury in ageing skeletal muscle.


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