Adult muscle satellite cells (MuSC) are stem cells in skeletal muscles and responsible for both embryonic and postnatal muscle growth and injury-induced muscle regeneration. Because of their abilities to repair damaged muscle and self-renew, MuSC have great therapeutic potentials for treatment of muscular dystrophies and other muscle diseases. However, due to limited MuSC present in muscles, an efficient way of expanding MuSC ex vivo is urgently needed. basic fibroblast growth factor (bFGF) is known to promote muscle satellite cell proliferation in culture and in vivo. We found that bFGF could effectively expand MuSC in vitro by transcriptionally up-regulating Pax7, a key marker for MuSC. We found that bFGF utilizes FGF receptor 1 and the extracellular signal-regulated kinase (ERK1/2)-m...[ Read more ]

Adult muscle satellite cells (MuSC) are stem cells in skeletal muscles and responsible for both embryonic and postnatal muscle growth and injury-induced muscle regeneration. Because of their abilities to repair damaged muscle and self-renew, MuSC have great therapeutic potentials for treatment of muscular dystrophies and other muscle diseases. However, due to limited MuSC present in muscles, an efficient way of expanding MuSC ex vivo is urgently needed. basic fibroblast growth factor (bFGF) is known to promote muscle satellite cell proliferation in culture and in vivo. We found that bFGF could effectively expand MuSC in vitro by transcriptionally up-regulating Pax7, a key marker for MuSC. We found that bFGF utilizes FGF receptor 1 and the extracellular signal-regulated kinase (ERK1/2)-mediated signaling pathway to activate Pax7 expression.

In addition, the JAK/STAT signaling pathways are known to play very important roles in regulating myoblasts proliferation and differentiation in vitro and in vivo. However, the role of JAK1 in regulating muscle regeneration in vivo remains unknown. In this study, we took advantage of the CreER/LoxP system and inducibly deleted JAK1 specifically in adult Pax7-expressing MuSC. By using these JAK1 inducible knockout (iKO) mice, we demonstrated that JAK1 is required for MuSC proliferation ex vivo and deletion of JAK1 delayed the muscle regeneration after CTX injury.