| Literature DB >> 24269820 |
Masanori A Murayama1, Shigeru Kakuta2, Takumi Maruhashi2, Kenji Shimizu2, Akimasa Seno3, Sachiko Kubo2, Nozomi Sato2, Shinobu Saijo4, Masahira Hattori5, Yoichiro Iwakura6.
Abstract
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.Entities:
Keywords: CTRP3; Collagen-induced arthritis; Rheumatoid arthritis
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Year: 2013 PMID: 24269820 DOI: 10.1016/j.bbrc.2013.11.040
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575