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Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway.

Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Research Abstract Details 

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  • Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Abstract Text:

    h yoshimuraH Yoshimura,k nakahamaK Nakahama,o safronovaO Safronova,n tanakaN Tanaka,t munetaT Muneta,i moritaI Morita,

    OBJECTIVE AND DESIGN: Transforming growth factor- beta (TGF-beta) has not only a fibrogenic role, but also monocyte/ macrophage chemotactic properties in a synovial joint. However, little is known about the effects of TGF-beta on monocyte chemoattractant protein-1 (MCP-1) expression in human synovial cells under inflammatory status. The aim of this study was to determine whether TGF-modulates MCP-1 production under the chronic inflammation, and to elucidate the cell signaling mechanism involved. MATERIALS AND METHODS: Human synovial cells were exposed to IL-1beta, which mimics the environment of chronic inflammation. Production of MCP-1 protein and expression of MCP-1 mRNA were determined by ELISA and real-time PCR. RESULTS: TGF-beta upregulated the expression of MCP-1 mRNA and protein with or without IL-1beta. TGF-beta and IL-1beta synergistically enhanced MCP-1 gene expression, and an AP-1 binding site was involved in the signal transduction. In addition, MEK inhibitor completely suppressed TGF-beta-induced MCP-1 production. CONCLUSIONS: TGF-beta and IL-1beta synergistically enhance MCP-1 gene expression through the activation of the MEK/ERK1/2 pathways, which leads to AP-1 activation. The impairment of MCP-1 regulation by TGF-beta in resident synovial cells might represent an important mechanism of chronic inflammation and tissue fibrosis in a synovial joint. MCP-1 should be considered a valid target for therapeutic intervention.

    Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Publishing Authors By Initials

    h yoshimuraH Yoshimura,k nakahamaK Nakahama,o safronovaO Safronova,n tanakaN Tanaka,t munetaT Muneta,i moritaI Morita,

    For similar abstracts research abstracts see: abstracts research

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    Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Inflammation research : official journal of the Eu

    VOLUME: 55

    Page Numbers: 543-9

    Journal Abbreviation: Inflamm. Res.

    ISSN: 1023-3830

    DAY: 15

    MONTH: Dec

    YEAR: 2006

    Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Information

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    LANGUAGE: eng

    NlmUniqueID: 9508160

    Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway. Keywords Mesh Terms:

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    Grant and Affiliation Information for Transforming growth factor-beta stimulates IL-1beta-induced monocyte chemoattractant protein-1 expression in human synovial cells via the ERK/AP-1 pathway.

    AFFILIATION: Department of Cellular Physiological Chemistry, Graduate School, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyo-ku, Tokyo, 113-8549, Japan.

    Country: Switzerland

    Switzerland Research PublicationSwitzerland Research Publication

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    MEDLINETA: Inflamm Res

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