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

E Angelino, S Reano, A Bollo, M Ferrara, M de Feudis, H Sustova, E Agosti, S Clerici, F Prodam, CL Tomasetto, A Graziani, N Filigheddu

Research output: Contribution to journalArticle

Abstract

Purpose: 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. Methods: To delineate the endogenous contribution of preproghrelin in muscle regeneration, we evaluated the repair process in Ghrl−/−mice upon CTX-induced injury. Results: Although muscles from Ghrl−/−mice do not visibly differ from WT muscles in term of weight, structure, and SCs content, muscle regeneration after CTX-induced injury is impaired in Ghrl−/−mice, indicating that ghrelin-derived peptides actively participate in muscle repair. Remarkably, the lack of ghrelin gene impacts SC self-renewal during regeneration. Conclusions: Although we cannot discern the specific Ghrl-derived peptide responsible for such activities, these data indicate that Ghrl contributes to a proper muscle regeneration. © 2018 Springer Science+Business Media, LLC, part of Springer Nature
Original languageEnglish
Pages (from-to)129-135
Number of pages7
JournalEndocrine
Volume62
Issue number1
DOIs
Publication statusPublished - 2018

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Ghrelin
Knockout Mice
Regeneration
Skeletal Muscle
Muscles
Peptides
Wounds and Injuries
Foster Home Care
Cell Self Renewal
Muscular Dystrophies
Myoblasts
Muscle Cells
Genes
Weights and Measures

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

In: Endocrine, Vol. 62, No. 1, 2018, p. 129-135.

Research output: Contribution to journalArticle

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 2018, 'Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal', Endocrine, vol. 62, no. 1, pp. 129-135. https://doi.org/10.1007/s12020-018-1606-4
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. / Ghrelin knockout mice display defective skeletal muscle regeneration and impaired satellite cell self-renewal. In: Endocrine. 2018 ; Vol. 62, No. 1. pp. 129-135.
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AB - Purpose: 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. Methods: To delineate the endogenous contribution of preproghrelin in muscle regeneration, we evaluated the repair process in Ghrl−/−mice upon CTX-induced injury. Results: Although muscles from Ghrl−/−mice do not visibly differ from WT muscles in term of weight, structure, and SCs content, muscle regeneration after CTX-induced injury is impaired in Ghrl−/−mice, indicating that ghrelin-derived peptides actively participate in muscle repair. Remarkably, the lack of ghrelin gene impacts SC self-renewal during regeneration. Conclusions: Although we cannot discern the specific Ghrl-derived peptide responsible for such activities, these data indicate that Ghrl contributes to a proper muscle regeneration. © 2018 Springer Science+Business Media, LLC, part of Springer Nature

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