tailieunhanh - Báo cáo y học: "Macrophage migration inhibitory factor enhances osteoclastogenesis through upregulation of RANKL expression from fibroblast-like synoviocytes in patients with rheumatoid arthriti"

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: Macrophage migration inhibitory factor enhances osteoclastogenesis through upregulation of RANKL expression from fibroblast-like synoviocytes in patients with rheumatoid arthritis. | Kim et al. Arthritis Research Therapy 2011 13 R43 http content 13 2 R43 RESEARCH ARTICLE Open Access Macrophage migration inhibitory factor enhances osteoclastogenesis through upregulation of RANKL expression from fibroblast-like synoviocytes in patients with rheumatoid arthritis Hae-Rim Kim13 Kyoung-Woon Kim23 Hong Geun Jung 3 Kwang-Sup Yoon3 Hye-Jwa Oh4 Mi-La Cho4 3 Sang-Heon Lee1 3 Abstract Introduction Macrophage migration inhibitory factor MIF is one of key regulators in acute and chronic immune-inflammatory conditions including rheumatoid arthritis RA . We examined the effect of MIF on osteoclastogenesis which is known to play a crucial role in bone destruction in RA. Methods The concentration of MIF and receptor activator of nuclear factor-KB ligand RANKL in the synovial fluid was measured by ELISA. MIF-induced RANKL expression of RA synovial fibroblasts was determined by real-time PCR and western blot. Osteoclastogenesis was analyzed in culture of human peripheral blood mononuclear cells PBMC with MIF. Osteoclastogenesis was also determined after co-cultures of rhMIF-stimulated RA synovial fibroblasts with human PBMC. Results Synovial fluid MIF concentration in RA patients was significantly higher than in osteoarthritis OA patients. The concentration of RANKL correlated with that of MIF in RA synovial fluids r P . MIF stimulated the expression of RANKL mRNA and protein in RA synovial fibroblasts which was partially reduced by blocking of interleukin IL -1p. Osteoclasts were differentiated from PBMC cultures with MIF and M-CSF even without RANKL. Osteoclastogenesis was increased after co-culture of MIF-stimulated RA synovial fibroblasts with PBMC and this effect was diminished by RANKL neutralization. Blocking of PI3 kinase p38 MAP kinase JAK-2 NF-kB and AP-1 also led to a marked reduction in RANKL expression and osteoclastogenesis. Conclusions The interactions among MIF synovial fibroblasts osteoclasts RANKL and IL- b have a