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软骨寡聚基质蛋白缺乏会促进胶原诱导性关节炎的早期发病和慢性发展。

Cartilage oligomeric matrix protein deficiency promotes early onset and the chronic development of collagen-induced arthritis.

作者信息

Geng Hui, Carlsen Stefan, Nandakumar Kutty Selva, Holmdahl Rikard, Aspberg Anders, Oldberg Ake, Mattsson Ragnar

机构信息

Department of Experimental Medical Sciences, BMC, Lund University, Lund, Sweden.

出版信息

Arthritis Res Ther. 2008;10(6):R134. doi: 10.1186/ar2551. Epub 2008 Nov 14.

DOI:10.1186/ar2551
PMID:19014566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2656236/
Abstract

INTRODUCTION

Cartilage oligomeric matrix protein (COMP) is a homopentameric protein in cartilage. The development of arthritis, like collagen-induced arthritis (CIA), involves cartilage as a target tissue. We have investigated the development of CIA in COMP-deficient mice.

METHODS

COMP-deficient mice in the 129/Sv background were backcrossed for 10 generations against B10.Q mice, which are susceptible to chronic CIA. COMP-deficient and wild-type mice were tested for onset, incidence, and severity of arthritis in both the collagen and collagen antibody-induced arthritis models. Serum anti-collagen II and anti-COMP antibodies as well as serum COMP levels in arthritic and wild-type mice were measured by enzyme-linked immunosorbent assay.

RESULTS

COMP-deficient mice showed a significant early onset and increase in the severity of CIA in the chronic phase, whereas collagen II-antibody titers were similar in COMP-deficient and wild-type controls. COMP antibodies were not found in wild-type mice. Finally, COMP-deficient and wild-type mice responded similarly to collagen antibody-induced arthritis, indicating no difference in how collagen II antibodies interact with COMP-deficient cartilage during the initial stages of arthritis.

CONCLUSIONS

COMP deficiency enhances the early onset and development of chronic arthritis but does not affect collagen II autoimmunity. These findings accentuate the importance of COMP in cartilage stability.

摘要

引言

软骨寡聚基质蛋白(COMP)是软骨中的一种同五聚体蛋白。关节炎的发展,如胶原诱导性关节炎(CIA),涉及软骨作为靶组织。我们研究了COMP缺陷小鼠中CIA的发展情况。

方法

将129/Sv背景的COMP缺陷小鼠与易患慢性CIA的B10.Q小鼠回交10代。在胶原和胶原抗体诱导的关节炎模型中,对COMP缺陷小鼠和野生型小鼠进行关节炎发病、发病率和严重程度的检测。通过酶联免疫吸附测定法测量关节炎小鼠和野生型小鼠血清中的抗胶原II和抗COMP抗体以及血清COMP水平。

结果

COMP缺陷小鼠在慢性期显示出CIA的明显早期发病和严重程度增加,而COMP缺陷小鼠和野生型对照中的胶原II抗体滴度相似。野生型小鼠中未发现COMP抗体。最后,COMP缺陷小鼠和野生型小鼠对胶原抗体诱导的关节炎反应相似,表明在关节炎初始阶段胶原II抗体与COMP缺陷软骨的相互作用没有差异。

结论

COMP缺陷会增强慢性关节炎的早期发病和发展,但不影响胶原II自身免疫。这些发现突出了COMP在软骨稳定性中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/1761480dd012/ar2551-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/4b1b53827d0a/ar2551-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/e49683223fa3/ar2551-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/a1987ad1ac7b/ar2551-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/4ca5fece20ee/ar2551-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/1761480dd012/ar2551-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/4b1b53827d0a/ar2551-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/e49683223fa3/ar2551-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/a1987ad1ac7b/ar2551-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/4ca5fece20ee/ar2551-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6476/2656236/1761480dd012/ar2551-5.jpg

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