Inhibition of endogenous TGF-β during experimental osteoarthritis prevents osteophyte formation and impairs cartilage repair

被引:174
作者
Scharstuhl, A [1 ]
Glansbeek, HL [1 ]
van Beuningen, HM [1 ]
Vitters, EL [1 ]
van der Kraan, PM [1 ]
van den Berg, WB [1 ]
机构
[1] Univ Nijmegen, Med Ctr, Dept Rheumatol, Rheumatol Res Lab, NL-6525 GA Nijmegen, Netherlands
关键词
D O I
10.4049/jimmunol.169.1.507
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Osteoarthritis has as main characteristics the degradation of articular cartilage and the formation of new bone at the joint edges, so-called osteophytes. In this study enhanced expression of TGF-beta1 and -beta3 was detected in developing osteophytes and articular cartilage during murine experimental osteoarthritis. To determine the role of endogenous TGF-beta on osteophyte formation and articular cartilage, TGF-beta activity was blocked via a scavenging soluble TGF-beta-RII. Our results clearly show that inhibition of endogenous TGF-beta nearly completely prevented osteophyte formation. In contrast, treatment with recombinant soluble TGF-beta-RII markedly enhanced articular cartilage proteoglycan loss and reduced the thickness of articular cartilage. In conclusion, we show for the first time that endogenous TGF-beta is a crucial factor in the process of osteophyte formation and has an important function in protection against cartilage loss.
引用
收藏
页码:507 / 514
页数:8
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