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.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Murayama MA,Kakuta S,Maruhashi T,Shimizu K,Seno A,Kubo S,Sato N,Saijo S,Hattori M,Iwakura Ydoi
10.1016/j.bbrc.2013.11.040subject
Has Abstractpub_date
2014-01-03 00:00:00pages
42-8issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(13)01922-0journal_volume
443pub_type
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