CTRP3 plays an important role in the development of collagen-induced arthritis in mice |
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Authors: | Masanori A. Murayama Shigeru Kakuta Takumi Maruhashi Kenji Shimizu Akimasa Seno Sachiko Kubo Nozomi Sato Shinobu Saijo Masahira Hattori Yoichiro Iwakura |
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Affiliation: | 1. Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo (IMSUT), Tokyo 108-8639, Japan;2. Department of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Chiba 277-0882, Japan;3. Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency (JST), Saitama 332-0012, Japan;4. PRESTO, JST, Saitama 332-0012, Japan |
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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. |
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Keywords: | Rheumatoid arthritis Collagen-induced arthritis CTRP3 |
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