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dc.rights.licenseopenen_US
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCARADU, Caroline
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGUY, Alexandre
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorJAMES, Chloé
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorREYNAUD, Annabel
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain-Pierre
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorRENAULT, Marie-Ange
dc.date.accessioned2020-11-24T15:17:31Z
dc.date.available2020-11-24T15:17:31Z
dc.date.issued2018
dc.identifier.issn1755-3245en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/20884
dc.description.abstractEnAims: Hedgehog (Hh) signalling has been shown to be re-activated in ischaemic tissues and participate in ischaemia-induced angiogenesis. Sonic Hedgehog (Shh) is upregulated by more than 80-fold in the ischaemic skeletal muscle, however its specific role in ischaemia-induced angiogenesis has not yet been fully investigated. The purpose of the present study was to investigate the role of endogenous Shh in ischaemia-induced angiogenesis. Methods and results: To this aim, we used inducible Shh knock-out (KO) mice and unexpectedly found that capillary density was significantly increased in re-generating muscle of Shh deficient mice 5 days after hind limb ischaemia was induced, demonstrating that endogenous Shh does not promote angiogenesis but more likely limits it. Myosin and MyoD expression were equivalent in Shh deficient mice and control mice, indicating that endogenous Shh is not required for ischaemia-induced myogenesis. Additionally, we observed a significant increase in macrophage infiltration in the ischaemic muscle of Shh deficient mice. Our data indicate that this was due to an increase in chemokine expression by myoblasts in the setting of impaired Hh signalling, using tissue specific Smoothened conditional KO mice. The increased macrophage infiltration in mice deficient for Hh signalling in myocytes was associated with increased VEGFA expression and a transiently increased angiogenesis, demonstrating that Shh limits inflammation and angiogenesis indirectly by signalling to myocytes. Conclusion: Although ectopic administration of Shh has previously been shown to promote ischaemia-induced angiogenesis, the present study reveals that endogenous Shh does not promote ischaemia-induced angiogenesis. On the contrary, the absence of Shh leads to aberrant ischaemic tissue inflammation and a transiently increased angiogenesis.
dc.language.isoENen_US
dc.subjectArticle RECHERCHE
dc.subject.enAnimal
dc.subject.enAnimals
dc.subject.enBlood Flow Velocity
dc.subject.enChemokines
dc.subject.enChemotaxis
dc.subject.enDisease Models
dc.subject.enHedgehog Proteins
dc.subject.enHindlimb
dc.subject.enInflammation
dc.subject.enIschemia
dc.subject.enKnockout
dc.subject.enMacrophages
dc.subject.enMice
dc.subject.enMuscle
dc.subject.enMyoblasts
dc.subject.enNeovascularization
dc.subject.enPhysiologic
dc.subject.enRegional Blood Flow
dc.subject.enSignal Transduction
dc.subject.enSkeletal
dc.subject.enTime Factors
dc.subject.enVascular Endothelial Growth Factor A
dc.title.enEndogenous Sonic Hedgehog limits inflammation and angiogenesis in the ischaemic skeletal muscle of mice
dc.typeArticle de revueen_US
dc.identifier.doi10.1093/cvr/cvy017en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed29365079en_US
bordeaux.journalCardiovascular Researchen_US
bordeaux.page759–770en_US
bordeaux.volume114en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue5en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
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