TRPV2 is essential for calcium signalling in the early stages of myogenesis

Skeletal muscle responds to stressors such as exercise and muscle injury by adaptive remodelling. The resilience of skeletal muscle involves not only mature muscle fibres but also the adjacent muscle satellite cells (MuSCs). We previously found that transient receptor potential vanilloid type 2 (TRPV2) is expressed in MuSCs and is essential for MuSC proliferation and activation in MuSC-specific conditional knockout mice. These mice show no mechanical-load-induced muscle hypertrophy and delayed injury-induced muscle regeneration. The effect of TRPV2 on Ca²⁺ signalling during early myogenesis is unknown; however, here, we demonstrate that tranilast, an inhibitor of TRPV2, suppressed IP₃R-derived Ca²⁺ oscillations in early myogenesis. The addition of adenovirus (Ad)-TRPV2 or Ad-Cre recombinase to floxed-TRPV2 cells modulated TRPV2 expression, and demonstrated the TRPV2 dependence of IP₃R and MEF2c expression, nuclear translocation of MEF2c, and Ca²⁺ oscillations. These findings indicate that TRPV2 regulates intracellular Ca²⁺ signalling during early myogenesis and highlight its potential as a target for the prevention and treatment of muscle disorders.