bFGF influences human articular chondrocyte differentiation

被引:43
|
作者
Schmal, H.
Zwingmann, J.
Fehrenbach, M.
Finkenzeller, G.
Stark, G. B.
Suedkamp, N. P.
Hartl, D.
Mehlhorn, A. T.
机构
[1] Univ Freiburg, Med Ctr, Dept Orthoped & Traumatol, D-79106 Freiburg, Germany
[2] Univ Freiburg, Med Ctr, Dept Plast & Hand Surg, D-79106 Freiburg, Germany
[3] Univ Munich, Dept Pediat, Munich, Germany
关键词
bFGF cartilage repair; chondrocytes; differentiation; proliferation;
D O I
10.1080/14653240601182846
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Background The possible functional role of basic fibroblast growth factor (bFGF) in regulating the mitotic and metabolic activity of primary human articular chondrocyres was investigated. Methods Chondrocytes were enzymatically isolated from femoral head cartilage, and were cultured in vitro in monolayer hFGF-dependent cell proliferation, production of collagen type II and aggrecan were monitored 10 days after isolation. Furthermore effect of bFGF on cell cycle, cell morphology, and mRNA expression of integrins and chondrogenic markers determined by real time PCR were analysed. Results bFGF concentrations in supernatants of primary human articular chondrocytes peaked immediately after isolation and then declined. In a dose-dependent manner, bFGF enhanced cell amplification viability. bFGF induced a decrease in the apoptotic cell population, while the number of proliferating cells remained unchanged. Supplementation of cell culture with bFGF reduced collagen type II mRNA by 49%, but increased expression of the integrin a, by 70%. bFGF did not significantly regulate the integrins alpha(1), alpha(5), alpha(10), alpha(v) and type I collagen. bFGF reduced the amount of collagen type II by 53%, which was correlated with diminished mRNA production. Monolayer cultured chondrocytes secreted significant amounts of aggrecan that decreased over time. Secretion of this cartilage-specific marker was further reduced by the addition of bFGF Discussion These findings highlight the potential role of bFGF as an endogenous chondrocyte mediator that can enhance cell amplification and regulate cell differentiation.
引用
收藏
页码:184 / 193
页数:10
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