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The role of p38 mitogen‐activated protein kinase in IL‐6 and IL‐8 production from the TNF‐α‐ or IL‐1β‐stimulated rheumatoid synovial fibroblasts
Author(s) -
Suzuki Masaki,
Tetsuka Toshifumi,
Yoshida Shinichi,
Watanabe Nobuyuki,
Kobayashi Masaaki,
Matsui Nobuo,
Okamoto Takashi
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01717-2
Subject(s) - p38 mitogen activated protein kinases , mitogen activated protein kinase , tumor necrosis factor alpha , interleukin , protein kinase a , ask1 , fibroblast , kinase , synovial membrane , map kinase kinase kinase , cancer research , microbiology and biotechnology , rheumatoid arthritis , medicine , mitogen activated protein kinase kinase , cytokine , chemistry , biology , biochemistry , in vitro
We examined the role of p38 mitogen‐activated protein (MAP) kinase in the tumor necrosis factor α (TNF‐α)‐ or interleukin‐1β (IL‐1β)‐induced production of interleukin‐6 (IL‐6) and interleukin‐8 (IL‐8) in fresh rheumatoid synovial fibroblast (RSF) cultures concomitantly with the induction of p38 MAP kinase activity. Pretreatment of RSF with a specific p38 MAP kinase inhibitor, SB203580, blocked the induction of IL‐6 and IL‐8 without affecting nuclear translocation of nuclear factor κB (NF‐κB) or IL‐6 and IL‐8 mRNA levels. These findings suggest that p38 MAP kinase inhibitor may have synergistic, rather than additive, effect for the treatment of rheumatoid arthritis.