作者: Adel Tekari , Reto Luginbuehl , Willy Hofstetter , Rainer J. Egli
DOI: 10.1371/JOURNAL.PONE.0120857
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摘要: Cartilage is a tissue with limited self-healing potential. Hence, cartilage defects require surgical attention to prevent or postpone the development of osteoarthritis. For cell-based repair strategies, in particular autologous chondrocyte implantation, articular chondrocytes are isolated from and expanded vitro increase number cells required for therapy. During expansion, lose competence autonomously form cartilage-like tissue, that absence exogenously added chondrogenic growth factors, such as TGF-βs. We hypothesized signaling elicited by autocrine and/or paracrine TGF-β essential formation alterations within pathway during expansion interfere this process. Primary bovine were harvested monolayer culture up passage six was investigated high density pellet cultures grown three weeks. Chondrocytes passages maintained potential autonomous formation. After passages, however, exogenous TGF-β1 induce tissue. When blocked inhibiting receptor 1 kinase, abrogated. At initiation culture, later showed levels transcripts coding receptors 2 TGF-β2 be three-, five- five-fold decreased, respectively, compared primary chondrocytes. In conclusion, dependent on induced TGF-β. propose decrease expression factor accounts activity hence loss