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实验性骨关节炎期间内源性转化生长因子-β的抑制可预防骨赘形成并损害软骨修复。

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

作者信息

Scharstuhl Alwin, Glansbeek Harrie L, van Beuningen Henk M, Vitters Elly L, van der Kraan Peter M, van den Berg Wim B

机构信息

Rheumatology Research Laboratory, Department of Rheumatology, University Medical Center, Nijmegen, The Netherlands.

出版信息

J Immunol. 2002 Jul 1;169(1):507-14. doi: 10.4049/jimmunol.169.1.507.

Abstract

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.

摘要

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。

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