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*
Department of Bioregulatory Medicine and Rheumatology, Tokyo Medical and Dental University Graduate School, Tokyo, Japan;
Department of Orthopedic Surgery, Osaka University Medical School, Osaka, Japan; and
Inflammation Research, Pharmacology Laboratories, Institute for Drug Discovery Research, Yamonouchi Pharmaceutical Co., Ltd., Ibaraki, Japan
Rheumatoid arthritis (RA) is characterized by proliferation of
synoviocytes that produce inflammatory cytokines and chemokines. The
expressed chemokines are thought to be involved in the migration of
inflammatory cells into the synovium. In this study we show that
CCL2/monocyte chemotactic protein-1, CCL5/RANTES, and CXCL12/stromal
cell-derived factor-1 enhanced IL-6 and IL-8 production by
fibroblast-like synoviocytes (FLS) from patients with RA, and their
corresponding receptors, CCR2, CCR5, and CXCR4, respectively, were
expressed by RA FLS. The chemokines stimulated RA FLS more effectively
than skin fibroblasts. Culture with CCL2 enhanced phosphorylation of
extracellular signal-related kinase 1 (ERK1) and ERK2, but not
phosphorylation of p38 or Src. Moreover, activation of ERK1/2 was
inhibited by pertussis toxin, a Gi-coupled protein
inhibitor, and RS-504393, CCR2 antagonist, suggesting that ERK1/2 was
activated by CCL2 via CCR2 and Gi-coupled protein. On the
other hand, CCL2, CCL5, and CXCL12 were expressed on RA FLS, and their
production was regulated by TNF-
, IL-1
, and TGF-1. Our results
indicate that the chemokines not only play a role in inflammatory cell
migration, but are also involved in the activation of FLS in RA
synovium, possibly in an autocrine or paracrine
manner.
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