Early response genes induced in chondrocytes stimulated with the inflammatory cytokine interleukin-1beta.docVIP

Early response genes induced in chondrocytes stimulated with the inflammatory cytokine interleukin-1beta.doc

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Early response genes induced in chondrocytes stimulated with the inflammatory cytokine interleukin-1beta

Available online /content/3/6/381 Research article Early response genes induced in chondrocytes stimulated with the inflammatory cytokine interleukin-1β Matthew P Vincenti* and Constance E Brinckerhoff*? *Department of Medicine, Dartmouth Medical School, Hanover, NH, USA ?Department of Biochemistry, Dartmouth Medical School, Hanover, NH, USA Correspondence: Matthew P Vincenti, Department of Medicine, Dartmouth Medical School, Hanover, NH, 03755, USA. Tel: +1 603 650 1607; fax: +1 603 650 1128; e-mail: Matthew.P.Vincenti@D Received: 31 May 2001 Arthritis Res 2001, 3:381-388 Revisions requested: 2 August 2001 Revisions received: 8 August 2001 Accepted: 14 August 2001 This article may contain supplementary data which can only be found online at /content/3/6/381 ? 2001 Vincenti and Brinckerhoff, licensee BioMed Central Ltd (Print ISSN 1465-9905; Online ISSN 1465-9913) Published: 18 September 2001 Abstract Recent work has established that IL-1β plays a central role in the inflammation and connective tissue destruction observed in both rheumatoid arthritis and osteoarthritis. These processes result from the ability of this inflammatory cytokine to activate expression of genes for neutral proteases, such as the matrix metalloproteinases. While IL-1β activates matrix metalloproteinase genes within several hours, it also activates immediate early genes, which are required for the later expression of matrix metalloproteinases and other arthritis-perpetuating genes, are also activated. To identify putative immediate early genes involved in IL-1β-mediated arthritic disease, a chondrocytic cell line (SW1353) was stimulated with this cytokine for 2 hours, total RNA was isolated, and expressed genes were identified by microarray analysis. This analysis identified alterations in the expression of multiple transcription factors, cytokines, growth factors and their receptors, adhesion molecules, proteases, and signa

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