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J Korean Rheum Assoc. 2005 Jun;12(2):73-82. Korean. Original Article.
Kang YM , Kim SI , Kim JS , You DW , Sa KH , Park EJ , Kim SU , Seo JS , Han SW , Nam EJ , Kyung HS , Kim MG , Kim IS , Kim JC .
Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea. ymkang@knu.ac.kr
Department of Internal Medicine, Pusan National University School of Medicine, Busan, Korea.
Departments of Orthopedic Surgery, Kyungpook National University School of Medicine, Daegu, Korea.
Departments of Immunology, Kyungpook National University School of Medicine, Daegu, Korea.
Departments of Biochemistry, Kyungpook National University School of Medicine, Daegu, Korea.
Abstract

OBJECTIVE: To investigate the expression pattern of transforming growth factor-beta-inducible gene-h3 (betaig-h3) within rheumatoid synovial tissue and the regulation of betaig-h3 synthesis in fibroblast-like synoviocyte (FLS). METHODS: Synovial tissues obtained from patients with rheumatoid arthritis and osteoarthritis were obtained during joint replacement surgery. betaig-h3 expression was evaluated with immunohistochemical stain. FLS was isolated from synovial tissues and stimulated with cytokines including TGF-beta, TNF-alpha, IL-1beta, IFN-gamma, IL-6, IL-4, and IL-10. betaig-h3 synthesis was measured using semiquantitative RT-PCR, ELISA, immunofluorescence stain, and flow cytometry. RESULTS: Expression of betaig-h3 was diffuse and abundant in both lining and sublining layers of rheumatoid synovium, which was more prominent than those of osteoarthritis. Production of betaig-h3 in FLS was regulated by TGF-beta1 in a dose-dependent manner and was highest at 5 ng/mL of TGF-beta1. TNF-alpha and IL-1beta upregulated the production of betaig-h3 from FLS synergistically with TGF-beta1 but other cytokines such as IL-4, IL-6, IL-10 did not affect. betaig-h3 synthesis was efficiently inhibited by dexamethasone at higher dose (100 nM) but not by cyclosporine-A. CONCLUSION: Production of betaig-h3, which is highly upregulated in rheumatoid synovitis, is differentially regulated by inflammatory cytokines.

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