title: Retinoic acid-inducible gene-I is induced by interleukin-1beta in cultured human gingival fibroblasts.
abstract: Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH box family protein, and details of its biological function are not known. We have studied the mechanism of the interleukin-1beta (IL-1beta)-induced RIG-I expression in human gingival fibroblasts in culture. We also addressed the possibility of enhanced expression of COX-2, RANTES and galectin-9 in fibroblasts overexpressed RIG-I. We stimulated cultured human gingival fibroblasts with IL-1beta and examined the expression of RIG-I mRNA and protein by reverse transcriptase-mediated polymerase chain reaction and Western blot analysis. The effect of cycloheximide, a protein synthesis inhibitor, on the IL-1beta-induced expression of RIG-I was examined. The expression of COX-2, RANTES, galectin-9 and monocyte chemoattractant protein-1 in gingival fibroblasts transfected with RIG-I cDNA was also examined. IL-1beta stimulated the expressions of mRNA and protein for RIG-I, in cultured fibroblasts, in a time- and concentration-dependent manner. Cycloheximide did not suppress the IL-1beta-induced RIG-I expression. Introduction of RIG-I cDNA into fibroblasts resulted in enhanced expression of COX-2 mRNA, and slightly enhanced the expression of mRNA for RANTES and galectin-9. In contrast, RIG-I overexpression did not alter the level of mRNA for monocyte chemoattractant protein-1. We conclude that IL-1beta stimulates RIG-I expression in human gingival fibroblasts.
authors.affiliation: Department of Dentistry and Oral Surgery, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan. sakaki@gaea.ocn.ne.jp
authors.forename: H
authors.initials: H
authors.lastname: Sakaki
authors.forename: T
authors.initials: T
authors.lastname: Imaizumi
authors.forename: T
authors.initials: T
authors.lastname: Matsumiya
authors.forename: A
authors.initials: A
authors.lastname: Kusumi
authors.forename: H
authors.initials: H
authors.lastname: Nakagawa
authors.forename: K
authors.initials: K
authors.lastname: Kubota
authors.forename: N
authors.initials: N
authors.lastname: Nishi
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: M
authors.initials: M
authors.lastname: Hirashima
authors.forename: K
authors.initials: K
authors.lastname: Satoh
authors.forename: H
authors.initials: H
authors.lastname: Kimura
mesh_terms: D015153:Blotting, Western; D018946:Chemokine CCL5 / Q000378:metabolism; D051546:Cyclooxygenase 2; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D037161:Galectins / Q000378:metabolism; D015870:Gene Expression; D005881:Gingiva / Q000166:cytology; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D008565:Membrane Proteins; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D020365:RNA Helicases / Q000235:genetics* / Q000378:metabolism; D011971:Receptors, Immunologic; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D018946:Chemokine CCL5; D037161:Galectins; D007375:Interleukin-1; D008565:Membrane Proteins; D011971:Receptors, Immunologic; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; C452820:RIGI protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases; D020365:RNA Helicases