Role of hypertrophic chondrocytes in the pathological remodeling of the osteochondral junction during osteoarthritis : involvement of SDF-1 in angiogenesis ; Rôle des chondrocytes hypertrophiques dans le remodelage pathologique de la jonction ostéochondrale au cours de l'arthrose : implication du SDF-1 dans l'angiogenèse
You can manage bookmarks using lists, please log in to your user account for this.
Media type:
E-Book
Title:
Role of hypertrophic chondrocytes in the pathological remodeling of the osteochondral junction during osteoarthritis : involvement of SDF-1 in angiogenesis ; Rôle des chondrocytes hypertrophiques dans le remodelage pathologique de la jonction ostéochondrale au cours de l'arthrose : implication du SDF-1 dans l'angiogenèse
Published:
[Erscheinungsort nicht ermittelbar]: HAL CCSD, 2021
Language:
French
Origination:
University thesis:
Dissertation, HAL CCSD, 2021
Footnote:
Description:
Osteoarthritis (OA) is the site of a reactivation of the endochondral ossification process, characterised by hypertrophic chondrocyte differentiation, cartilage mineralisation, osteochondral angiogenesis and subchondral bone remodeling. Osteochondral angiogenesis may play a central role in the progression of OA, but the molecular actors responsible for cartilage vascularisation are still unknown. We believe that hypertrophic differentiation of chondrocytes plays a pivotal role in osteochondral junction remodeling and particularly in osteochondral angiogenesis, through increased synthesis of angiogenic factors. We showed that hypertrophic chondrocytes has a transcriptomic signature in favour of a pro-angiogenic role and confirmed this potential using different functional assays of angiogenesis in vitro (adhesion of endothelial cells to chondrocyte extracellular matrices, proliferation, migration and tube formation in response to stimulation by chondrocyte conditioned media). A study of the chondrocyte secretome identified Stromal-Derived Factor 1 (SDF-1) as a potential source of the pro-angiogenic effects of hypertrophic chondrocytes. We showed that blocking the SDF-1/CXCR4 axis by AMD3100 abolished the effects of hypertrophic chondrocytes on migration and tubulogenesis. Differentiation of pre-hypertrophic chondrocytes into hypertrophic chondrocytes could therefore promote pathological vascularisation of cartilage by producing SDF-1. ; L'arthrose (OA) est le siège d'une réactivation du processus d'ossification endochondrale, caractérisé par une différenciation hypertrophique des chondrocytes, une minéralisation du cartilage, une angiogenèse ostéochondrale et un remodelage de l'os sous-chondral. L'angiogenèse ostéochondrale pourrait jouer un rôle central dans la progression de l'OA mais les acteurs moléculaires responsables de la vascularisation du cartilage sont encore méconnus. Nous pensons que la différenciation hypertrophique des chondrocytes joue un rôle moteur dans le remodelage de la jonction ostéochondrale ...