CTRP3 plays an important role in the development of collagen-induced arthritis in mice

被引：70

作者：

Murayama, Masanori A. ^{[1
,2
,3
]}

Kakuta, Shigeru ^{[1
]}

Maruhashi, Takumi ^{[1
]}

Shimizu, Kenji ^{[1
]}

Seno, Akimasa ^{[1
,2
]}

Kubo, Sachiko ^{[1
]}

Sato, Nozomi ^{[1
]}

Saijo, Shinobu ^{[1
,4
]}

Hattori, Masahira ^{[2
]}

Iwakura, Yoichiro ^{[1
,2
,3
]}

机构：

[1] Univ Tokyo IMSUT, Inst Med Sci, Ctr Expt Med & Syst Biol, Tokyo 1088639, Japan

[2] Univ Tokyo, Grad Sch Frontier Sci, Dept Computat Biol, Kashiwa, Chiba 2770882, Japan

[3] Japan Sci & Technol Agcy JST, Core Res Evolut Sci & Technol, Kawaguchi, Saitama 3320012, Japan

[4] JST, PRESTO, Kawaguchi, Saitama 3320012, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 443卷 / 01期

关键词：

Rheumatoid arthritis; Collagen-induced arthritis; CTRP3; RESEMBLING RHEUMATOID-ARTHRITIS; ADIPOSE-TISSUE; COMPLEMENT; ADIPONECTIN; ANTAGONIST; DEFICIENT; INDUCTION; PROTOCOL; PARALOG; PATHWAY;

D O I：

10.1016/j.bbrc.2013.11.040

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease exhibited most commonly in joints. We found that the expression of C1qtnf3, which encodes C1q/TNF-related protein 3 (CTRP3), was highly increased in two mouse RA models with different etiology. To elucidate the pathogenic roles of CTRP3 in the development of arthritis, we generated C1qtnf3(-/-) mice and examined the development of collagen-induced arthritis in these mice. We found that the incidence and severity score was higher in C1qtnf3(-/-) mice compared with wild-type (WT) mice. Histopathology of the joints was also more severe in C1qtnf3(-/-) mice. The levels of antibodies against type II collagen and pro-inflammatory cytokine mRNAs in C1qtnf3(-/-) mice were higher than WT mice. These observations indicate that CTRP3 plays an important role in the development of autoimmune arthritis, suggesting CTRP3 as a possible medicine to treat RA. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.

引用

页码：42 / 48

页数：7

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