登录 | 注册 English | 中文版

首页 科室概况 医疗服务 科研动态 教学天地 关于我们
当前位置是: 首页 > 科研动态 > 专业新闻 >
>专业新闻

我科客座教授曹旭课题组关于骨关节炎病理机制的研究论文于2013年在Nat Med上发表

来源:解剖生理科时间:2014-09-29 17:18:15作者:系统管理员点击数:

Nat Med.2013 Jun;19(6):704-12. doi: 10.1038/nm.3143. Epub 2013 May 19.

Inhibition of TGF-β signaling in mesenchymal stem cells of subchondral bone attenuates osteoarthritis.

Zhen G, Wen C, Jia X, Li Y, Crane JL, Mears SC, Askin FB, Frassica FJ, Chang W, Yao J, Carrino JA, Cosgarea A, Artemov D, Chen Q, Zhao Z, Zhou X, Riley L, Sponseller P, Wan M, Lu WW, Cao X.

Department of Orthopaedic Surgery, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.

Abstract

Osteoarthritis is a highly prevalent and debilitating joint disorder. There is no effective medical therapy for the condition because of limited understanding of its pathogenesis. We show that transforming growth factor β1 (TGF-β1) is activated in subchondral bone in response to altered mechanical loading in an anterior cruciate ligament transection (ACLT) mouse model of osteoarthritis. TGF-β1 concentrations are also high in subchondral bone from humans with osteoarthritis. High concentrations of TGF-β1 induced formation of nestin-positive mesenchymal stem cell (MSC) clusters, leading to formation of marrow osteoid islets accompanied by high levels of angiogenesis. We found that transgenic expression of active TGF-β1 in osteoblastic cells induced osteoarthritis, whereas inhibition of TGF-β activity in subchondral bone attenuated the degeneration of articular cartilage. In particular, knockout of the TGF-β type II receptor (TβRII) in nestin-positive MSCs led to less development of osteoarthritis relative to wild-type mice after ACLT. Thus, high concentrations of active TGF-β1 in subchondral bone seem to initiate the pathological changes of osteoarthritis, and inhibition of this process could be a potential therapeutic approach to treating this disease.

版权所有:第四军医大学口腔学院解剖生理科

联系电话:029-84776143

学院地址:西安市长乐中路145号