tailieunhanh - Báo cáo y học: "Potential role and mechanism of IFN-gamma inducible protein-10 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in rheumatoid arthritis"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Potential role and mechanism of IFN-gamma inducible protein-10 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in rheumatoid arthritis. | Lee et al. Arthritis Research Therapy 2011 13 R104 http content 13 3 R104 RESEARCH ARTICLE Open Access Potential role and mechanism of IFN-gamma inducible protein-10 on receptor activator of nuclear factor kappa-B ligand RANKL expression in rheumatoid arthritis 12 2 111 Eun Young Lee MiRan Seo Yong-Sung Juhnn Jeong Yeon Kim Yoo Jin Hong Yun Jong Lee Eun Bong Lee 1 and Yeong Wook Song1 Abstract Introduction IFN-gamma inducible protein-10 CXCL10 a member of the CXC chemokine family and its receptor CXCR3 contribute to the recruitment of T cells from the blood stream into the inflamed joints and have a crucial role in perpetuating inflammation in rheumatoid arthritis RA synovial joints. Recently we showed the role of CXCL10 on receptor activator of nuclear factor kappa-B ligand RANKL expression in an animal model of RA and suggested the contribution to osteoclastogenesis. We tested the effects of CXCL10 on the expression of RANKL in RA synoviocytes and T cells and we investigated which subunit of CXCR3 contributes to RANKL expression by CXCL10. Methods Synoviocytes derived from RA patients were kept in culture for 24 hours in the presence or absence of TNF-a. CXCL10 expression was measured by reverse transcriptase polymerase chain reaction RT-PCR of cultured synoviocytes. Expression of RANKL was measured by RT-PCR and western blot in cultured synoviocytes with or without CXCL10 and also measured in Jurkat Hut 78 T cells and CD4 T cells in the presence of CXCL10 or dexamethasone. CXCL10 induced RANKL expression in Jurkat T cells was tested upon the pertussis toxin PTX an inhibitor of Gi subunit of G protein coupled receptor GPCR . The synthetic siRNA for Gai2 was used to knock down gene expression of respective proteins. Results CXCL10 expression in RA synoviocytes was increased by TNF-a. CXCL10 slightly increased RANKL expression in RA synoviocytes but markedly increased RANKL expression in Jurkat Hut 78 T cell or CD4 T cell. CXCL10 augmented .

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