title: Tumor-necrosis factor-alpha induces retinoic acid-inducible gene-I in rheumatoid fibroblast-like synoviocytes.
abstract: Tumor-necrosis factor-alpha (TNF-alpha) is a potent proinflammtory cytokine and a key molecule in the pathogenesis of rheumatoid arthritis (RA). Retinoic acid-inducible gene-I (RIG-I) is a DExH box protein, which is known to play a role in the inflammatory and immune reactions. We previously reported about potential involvement of RIG-I in synovial inflammation in RA. In the present study, we demonstrated the expression of RIG-I in fibroblast-like synoviocytes stimulated with TNF-alpha. RNA interference against interferon (IFN)-beta abolished the TNF-alpha-induced RIG-I expression. In addition, knockdown of RIG-I partially inhibited the TNF-alpha-induced expression of CC chemokine ligand (CCL) 5, a chemokine with chemotactic activity toward lymphocytes and monocytes. These findings suggest that the TNF-alpha/IFN-beta/RIG-I/CCL5 pathway may be involved in the pathogenesis of synovial inflammation in RA.
authors.affiliation: Department of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan. timaizum@cc.hirosaki-u.ac.jp
authors.forename: Tadaatsu
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Tomoh
authors.initials: T
authors.lastname: Matsumiya
authors.forename: Hidemi
authors.initials: H
authors.lastname: Yoshida
authors.forename: Takuya
authors.initials: T
authors.lastname: Naraoka
authors.forename: Ryoko
authors.initials: R
authors.lastname: Uesato
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Ishibashi
authors.forename: Ken
authors.initials: K
authors.lastname: Ota
authors.forename: Satoshi
authors.initials: S
authors.lastname: Toh
authors.forename: Shinsaku
authors.initials: S
authors.lastname: Fukuda
authors.forename: Kei
authors.initials: K
authors.lastname: Satoh
mesh_terms: D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D002135:Calcium-Binding Proteins / Q000276:immunology / Q000378:metabolism; D002478:Cells, Cultured; D018946:Chemokine CCL5 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D025461:Feedback, Physiological / Q000235:genetics / Q000276:immunology; D005347:Fibroblasts / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D016899:Interferon-beta / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D034622:RNA Interference / Q000276:immunology; D034741:RNA, Small Interfering; D018168:Receptors, Retinoic Acid / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D000071999:S100 Calcium-Binding Protein A4; D015398:Signal Transduction / Q000276:immunology; D013582:Synovial Fluid / Q000276:immunology / Q000378:metabolism*; D015533:Transcriptional Activation / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology* / Q000378:metabolism
chemical_list: C483024:CCL5 protein, human; D002135:Calcium-Binding Proteins; D018946:Chemokine CCL5; C437968:PLAAT4 protein, human; D034741:RNA, Small Interfering; D018168:Receptors, Retinoic Acid; D000071999:S100 Calcium-Binding Protein A4; D014409:Tumor Necrosis Factor-alpha; C077591:S100A4 protein, human; D016899:Interferon-beta