Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal.

Fiche publication

Date publication

octobre 2018

Journal

Endocrine

Auteurs

Membres identifiés du Cancéropôle Est :
Dr TOMASETTO Catherine

Tous les auteurs :
Angelino E, Reano S, Bollo A, Ferrara M, De Feudis M, Sustova H, Agosti E, Clerici S, Prodam F, Tomasetto CL, Graziani A, Filigheddu N

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/29846901

Résumé

Muscle regeneration depends on satellite cells (SCs), quiescent precursors that, in consequence of injury or pathological states such as muscular dystrophies, activate, proliferate, and differentiate to repair the damaged tissue. A subset of SCs undergoes self-renewal, thus preserving the SC pool and its regenerative potential. The peptides produced by the ghrelin gene, i.e., acylated ghrelin (AG), unacylated ghrelin (UnAG), and obestatin (Ob), affect skeletal muscle biology in several ways, not always with overlapping effects. In particular, UnAG and Ob promote SC self-renewal and myoblast differentiation, thus fostering muscle regeneration.