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A role of monocyte chemoattractant protein‐4 (MCP‐4)/CCL13 from chondrocytes in rheumatoid arthritis
Author(s) -
Iwamoto Takuji,
Okamoto Hiroshi,
Kobayashi Shu,
Ikari Katsunori,
Toyama Yoshiaki,
Tomatsu Taisuke,
Kamatani Naoyuki,
Momohara Shigeki
Publication year - 2007
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2007.06013.x
Subject(s) - ccl13 , monocyte , cancer research , tumor necrosis factor alpha , medicine , immunology , inflammation , chemokine , chemokine receptor
We studied the role of monocyte chemoattractant (MCP)‐4/CCL13 in the pathogenesis of rheumatoid arthritis (RA). MCP‐4 was highly expressed in cartilage from RA patients. Interferon‐γ significantly stimulated MCP‐4/CCL13 production in human chondrocytes, and this effect was enhanced in combination with interleukin‐1β or tumor necrosis factor‐α. MCP‐4/CCL13 induces the phosphorylation of extracellular signal‐regulated kinase in fibroblast‐like synoviocytes and activates cell proliferation, and PD98059 completely inhibits these effects. These data suggest that interferon‐γ in combination with interleukin‐1β/tumor necrosis factor‐α activates the production of MCP‐4/CCL13 from chondrocytes in RA joints, and that secreted MCP‐4/CCL13 enhances fibroblast‐like synoviocyte proliferation by activating the extracellular signal‐regulated kinase mitogen‐activated protein kinase cascade.