| First Author | Murayama MA | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 443 |
| Issue | 1 | Pages | 42-8 |
| PubMed ID | 24269820 | Mgi Jnum | J:211893 |
| Mgi Id | MGI:5576850 | Doi | 10.1016/j.bbrc.2013.11.040 |
| Citation | Murayama MA, et al. (2014) CTRP3 plays an important role in the development of collagen-induced arthritis in mice. Biochem Biophys Res Commun 443(1):42-8 |
| abstractText | 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. |
