Scharstuhl Alwin, Glansbeek Harrie L, van Beuningen Henk M, Vitters Elly L, van der Kraan Peter M, van den Berg Wim B
Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center, Nijmegen, The Netherlands.
J Immunol. 2002 Jul 1;169(1):507-14. doi: 10.4049/jimmunol.169.1.507.
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.
骨关节炎的主要特征是关节软骨退化以及在关节边缘形成新骨,即所谓的骨赘。在本研究中,在小鼠实验性骨关节炎期间,在发育中的骨赘和关节软骨中检测到TGF-β1和-β3的表达增强。为了确定内源性TGF-β在骨赘形成和关节软骨中的作用,通过清除可溶性TGF-β-RII来阻断TGF-β活性。我们的结果清楚地表明,内源性TGF-β的抑制几乎完全阻止了骨赘的形成。相反,用重组可溶性TGF-β-RII治疗显著增强了关节软骨蛋白聚糖的丢失并降低了关节软骨的厚度。总之,我们首次表明内源性TGF-β是骨赘形成过程中的关键因素,并且在防止软骨丢失方面具有重要作用。