A role of monocyte chemoattractant protein-4 (MCP-4)/CCL13 from chondrocytes in rheumatoid arthritis

被引：29

作者：

Iwamoto, Takuji

Okamoto, Hiroshi

Kobayashi, Shu

Ikari, Katsunori

Toyama, Yoshiaki

Tomatsu, Taisuke

Kamatani, Naoyuki

Momohara, Shigeki

机构：

[1] Tokyo Womens Med Univ, Inst Rheumatol, Shinjuku Ku, Tokyo 162, Japan

[2] Keio Univ, Sch Med, Dept Orthoped Surg, Tokyo, Japan

来源：

FEBS JOURNAL | 2007年 / 274卷 / 18期

关键词：

chondrocytes; extracellular signal-regulated kinase (ERK); monocyte chemoattractant protein-4 (MCP-4); CCL13; rheumatoid arthritis;

D O I：

10.1111/j.1742-4658.2007.06013.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

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-gamma significantly stimulated MCP-4/CCL13 production in human chondrocytes, and this effect was enhanced in combination with interleukin-1 beta or tumor necrosis factor-alpha. 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-gamma in combination with interleukin-1 beta/tumor necrosis factor-alpha 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.

引用

页码：4904 / 4912

页数：9

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