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Capsaicin mimics mechanical load-induced intracellular signaling events: Involvement of TRPV1-mediated calcium signaling in induction of skeletal muscle hypertrophy

Mechanical load-induced intracellular signaling events are important for subsequent skeletal muscle hypertrophy. We previously showed that load-induced activation of the cation channel TRPV1 caused an increase in intracellular calcium concentrations ([Ca(2+)](i)) and that this activated mammalian ta...

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Detalles Bibliográficos
Autores principales: Ito, Naoki, Ruegg, Urs T., Kudo, Akira, Miyagoe-Suzuki, Yuko, Takeda, Shin’ichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710350/
https://www.ncbi.nlm.nih.gov/pubmed/23584166
http://dx.doi.org/10.4161/chan.24583
Descripción
Sumario:Mechanical load-induced intracellular signaling events are important for subsequent skeletal muscle hypertrophy. We previously showed that load-induced activation of the cation channel TRPV1 caused an increase in intracellular calcium concentrations ([Ca(2+)](i)) and that this activated mammalian target of rapamycin (mTOR) and promoted muscle hypertrophy. However, the link between mechanical load-induced intracellular signaling events, and the TRPV1-mediated increases in [Ca(2+)](i) are not fully understood. Here we show that administration of the TRPV1 agonist, capsaicin, induces phosphorylation of mTOR, p70S6K, S6, Erk1/2 and p38 MAPK, but not Akt, AMPK or GSK3β. Furthermore, the TRPV1-induced phosphorylation patterns resembled those induced by mechanical load. Our results continue to highlight the importance of TRPV1-mediated calcium signaling in load-induced intracellular signaling pathways.