Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration

David Hardy (1) , Mylène Fefeu (1) , Aurore Besnard (1) , David Briand (1) , Pamela Gasse (2) , Fernando Arenzana-Seisdedos (2) , Pierre Rocheteau (1, 3) , Fabrice Chrétien (1, 3)

1 Neuropathologie expérimentale - Experimental neuropathology
2 Pathogénie Virale Moléculaire
3 Centre Hospitalier Sainte Anne [Paris]

During muscle regeneration, the chemokine CXCL12 (SDF-1) and the synthesis of some specific heparan sulfates (HS) have been shown to be critical. CXCL12 activity has been shown to be heavily influenced by its binding to extracellular glycosaminoglycans (GAG) by modulating its presentation to its receptors and by generating haptotactic gradients. Although CXCL12 has been implicated in several phases of tissue repair, the influence of GAG binding under HS influencing conditions such as acute tissue destruction remains understudied.

Mots clés: Skeletal muscle; Vasculogenesis; Angiogenesis; CXCL12; Endothelial cells; Fibrosis; Heparan sulfates; Muscle stem cells; Regeneration

Domaines: Biologie cellulaire; Interactions cellulaires [q-bio.CB]; Biologie du développement

David Hardy, Mylène Fefeu, Aurore Besnard, David Briand, Pamela Gasse, et al.. Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration. Skeletal Muscle, 2019, 9 (1), pp.25. ⟨10.1186/s13395-019-0210-5⟩. ⟨pasteur-02861879⟩