Chemokine expression and control of muscle cell migration during myogenesis

Abstract

SummaryAdult regenerative myogenesis is vital for restoring normal tissue structure after muscle injury. Muscle regeneration is dependent on progenitor satellite cells, which proliferate in response to injury, and their progeny differentiate and undergo cell-cell fusion to form regenerating myofibers. Myogenic progenitor cells must be precisely regulated and positioned for proper cell fusion to occur. Chemokines are secreted proteins that share both leukocyte chemoattractant and cytokine-like behavior and affect the physiology of a number of cell types. We investigated the steady-state mRNA levels of 84 chemokines, chemokine receptors and signaling molecules, to obtain a comprehensive view of chemokine expression by muscle cells during myogenesis in vitro. A large number of chemokines and chemokine receptors were expressed by primary mouse muscle cells, especially during times of extensive cell-cell fusion. Furthermore, muscle cells exhibited different migratory behavior throughout myogenesis in vitro. One receptor-ligand pair, CXCR4-SDF-1 (CXCL12), regulated migration of both proliferating and terminally differentiated muscle cells, and was necessary for proper fusion of muscle cells. Given the large number of chemokines and chemokine receptors directly expressed by muscle cells, these proteins might have a greater role in myogenesis than previously appreciated.

An NF-κB - EphrinA5-Dependent Communication between NG2+ Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates

“…This regulation was selective to the p65 subunit, since similar differences in myoblast migration were not observed between p50 +/+ and p50 −/− NG2 + cultures (Figure S2A). We also found that migration was more efficient when myoblasts were exposed to myotubes rather than an empty chamber (Figure S2B), consistent with the notion that myotubes secrete chemotactic factors to stimulate myoblast motility (Griffin et al, 2010). We previously demonstrated that p65 regulation of the inducible nitric oxide synthase gene (iNOS) and secretion of nitric oxide (NO) from stromal fibroblasts promotes myoblast nuclear accretion to myofibers (Dahlman et al, 2010).…”

“…A further role for the HGF/c-MET axis has been studied in adult muscles undergoing regeneration (Webster and Fan, 2013), but whether this ligand-receptor signaling pathway functions in newborn muscles to stimulate myoblast proliferation or migration is not known. Additional factors, CXCL12 and odorant receptor, MOR23, have also been shown to contribute to myoblast migration during in vitro myogenesis and adult muscle regeneration (Griffin et al, 2010; Griffin et al, 2009), but whether their activities are relevant in promoting myoblasts to the ends of growing fibers in newborn muscles will require additional investigation.…”

Mathematical modelling of atheroma plaque formation and development in coronary arteries

“…The convection is disregarded due to the large size of the SMCs, and the diffusion is disregarded because these cells migrate instead of being spread by diffusion. Furthermore, synthetic SMCs are induced into the intima by the chemoattractant (cytokines), m Ss being the migration rate of these cells [63].…”

Identification and functional characterization of TRPA1 in human myoblasts

“…As the migration of myoblasts is a crucial step in the beginning of muscle repair [20], we investigated the impact of TRPA1 stimulation on the migration activity of human myoblasts. Cells were embedded in a 3D collagen layer to provide an environment more similar to an in vivo situation than in classical migration experiments.…”