Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration
CXCL12突变小鼠血管生成缺陷损害骨骼肌再生
作者: David HardyMylène FefeuAurore BesnardDavid BriandPaméla GasseFernando Arenzana-SeisdedosPierre RocheteauFabrice Chrétien
作者单位: 10000 0001 2353 6535, grid.428999.7, Experimental Neuropathology Unit, Institut Pasteur, 75015, Paris, France
20000 0001 2353 6535, grid.428999.7, Viral Pathogenesis Unit, Institut Pasteur, 75015, Paris, France
30000 0001 2200 9055, grid.414435.3, Service Hospitalo-Universitaire de Psychiatrie, Centre Hospitalier Sainte Anne, 75014, Paris, France
40000 0001 2188 0914, grid.10992.33, Paris Descartes University, Sorbonne Paris Cité, 75006, Paris, France
50000 0001 2200 9055, grid.414435.3, Service Hospitalo-Universitaire de Neuropathologie, Centre Hospitalier Sainte Anne, 75014, Paris, France
刊名: Skeletal Muscle, 2019, Vol.9 (1), pp.19-32
来源数据库: Springer Nature Journal
DOI: 10.1186/s13395-019-0210-5
关键词: Muscle stem cellsEndothelial cellsCXCL12Heparan sulfatesSkeletal muscleRegenerationAngiogenesisVasculogenesisFibrosis
英文摘要: Abstract(#br)Background(#br)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. Methods(#br)To investigate the role of the CXCL12/HS proteoglycan interactions in the pathophysiology of muscle regeneration, we performed two models of muscle injuries (notexin and freeze injury) in mutant CXCL12Gagtm/Gagtm...
全文获取路径: Springer Nature  (合作)
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