Fiche publication
Date publication
mars 2016
Journal
Cell reports
Auteurs
Membres identifiés du Cancéropôle Est :
Dr OREND Gertraud
Tous les auteurs :
Tierney MT, Gromova A, Sesillo FB, Sala D, Spenlé C, Orend G, Sacco A
Lien Pubmed
Résumé
Muscle stem cells (MuSCs) exhibit distinct behavior during successive phases of developmental myogenesis. However, how their transition to adulthood is regulated is poorly understood. Here, we show that fetal MuSCs resist progenitor specification and exhibit altered division dynamics, intrinsic features that are progressively lost postnatally. After transplantation, fetal MuSCs expand more efficiently and contribute to muscle repair. Conversely, niche colonization efficiency increases in adulthood, indicating a balance between muscle growth and stem cell pool repopulation. Gene expression profiling identified several extracellular matrix (ECM) molecules preferentially expressed in fetal MuSCs, including tenascin-C, fibronectin, and collagen VI. Loss-of-function experiments confirmed their essential and stage-specific role in regulating MuSC function. Finally, fetal-derived paracrine factors were able to enhance adult MuSC regenerative potential. Together, these findings demonstrate that MuSCs change the way in which they remodel their microenvironment to direct stem cell behavior and support the unique demands of muscle development or repair.
Mots clés
Animals, Collagen Type VI, genetics, Embryo, Mammalian, Extracellular Matrix, metabolism, Fetus, Fibronectins, genetics, Gene Expression Regulation, Developmental, Genes, Reporter, Luciferases, genetics, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Transgenic, Muscle Development, genetics, Muscle, Skeletal, cytology, Myoblasts, Skeletal, cytology, Signal Transduction, Stem Cell Transplantation, Tenascin, genetics, Wound Healing, physiology
Référence
Cell Rep. 2016 Mar;14(8):1940-52
