Myogenic-specific ablation of Fgfr1 impairs FGF2-mediated proliferation of satellite cells at the myofiber niche but does not abolish the capacity for muscle regeneration

摘要: Skeletal muscle satellite cells (SCs) are Pax7+ myogenic stem that reside between the basal lamina and plasmalemma of myofiber. In mature muscles, SCs typically quiescent, but can be activated in response to injury. Depending on magnitude tissue trauma, may divide minimally repair subtle damage within individual myofibers or produce a larger progeny pool forms new cases overt SC transition through proliferation, differentiation renewal is governed by molecular blueprint as well extracellular milieu at niche. particular, role fibroblast growth factor (FGF) family regulating during aging recognized. Of several FGFs shown affect SCs, FGF1, FGF2 FGF6 proteins have been documented adult skeletal muscle. These prototypic paracrine transmit their mitogenic effect FGFRs, which transmembrane tyrosine kinase receptors. Using mouse model, we show here four only Fgfr1 Fgfr4 expressed relatively high levels quiescent proliferating progeny. To further investigate FGFR1 myogenesis, employed genetic (Cre/loxP) approach for myogenic-specific (MyoDCre-driven) ablation Fgfr1. Neither histology nor regeneration following cardiotoxin-induced injury were overtly affected Fgfr1-ablated mice. This suggests not obligatory performance this acute trauma where compensatory factor/cytokine regulatory cascades exist. However, drastically repressed isolated prepared from Collectively, our study indicates important FGF-mediated proliferation its compensated FGFR4 also highly SCs.