Skeletal muscle adaptation in response to mechanical stress in p130cas-/- mice.

Takayuki Akimoto, Kanako Okuhira, Katsuji Aizawa, Shogo Wada, Hiroaki Honda, Toru Fukubayashi, Takashi Ushida

Division of Regenerative Medical Engineering, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, Tokyo 113-0033, Japan. akimoto@m.u-tokyo.ac.jp

American journal of physiology. Cell physiology 2013 Mar

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Mammalian skeletal muscles undergo adaptation in response to changes in the functional demands upon them, involving mechanical-stress-induced cellular signaling called "mechanotransduction." We hypothesized that p130Cas, which is reported to act as a mechanosensor that transduces mechanical extension into cellular signaling, plays an important role in maintaining and promoting skeletal muscle adaptation in response to mechanical stress via the p38 MAPK signaling pathway. We demonstrate that muscle-specific p130Cas-/- mice express the contractile proteins normally in skeletal muscle. Furthermore, muscle-specific p130Cas-/- mice show normal mechanical-stress-induced muscle adaptation, including exercise-induced IIb-to-IIa muscle fiber type transformation and hypertrophy. Finally, we provide evidence that exercise-induced p38 MAPK signaling is not impaired by the muscle-specific deletion of p130Cas. We conclude that p130Cas plays a limited role in mechanical-stress-induced skeletal muscle adaptation.

Citation

Takayuki Akimoto, Kanako Okuhira, Katsuji Aizawa, Shogo Wada, Hiroaki Honda, Toru Fukubayashi, Takashi Ushida. Skeletal muscle adaptation in response to mechanical stress in p130cas-/- mice. American journal of physiology. Cell physiology. 2013 Mar;304(6):C541-7