Laboratory study reveals mechanosensitive calcium fluctuations drive muscle stem cell activation in mice, highlighting biomechanical pathways in muscle regeneration and aging.
Key Points
To characterize calcium ion (Ca2+) mobilization in muscle satellite cells (MuSCs) and delineate the mechanisms controlling these signals during myofiber regeneration.
Isolated MuSCs from mice subjected to cardiotoxin-induced muscle injury, including aged and dystrophic models.
Profiled Ca2+ dynamics across quiescent, activated, and proliferative MuSC stages using both chemical and genetically encoded Ca2+ indicators.
Assessed the contributions of mechanosensitive ion channels, specifically PIEZO1 and TRPM7, to Ca2+ fluctuations and cell motility.
Spontaneous Ca2+ fluctuations increased in both frequency and amplitude as MuSCs transitioned into activated and proliferative states compared with quiescence.
Ca2+ fluctuation frequency and amplitude were elevated to a greater extent in MuSCs from dystrophic and aged mice relative to healthy controls.
Mechanosensitive ion channels PIEZO1 and TRPM7 mediated these Ca2+ signals and facilitated MuSC migration during tissue repair.