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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Selective Inhibitor of p38 Mitogen-Activated Protein Kinase Inhibits Lipopolysaccharide-Induced Interleukin-8 Expression in Human Pulmonary Vascular Endothelial Cells

Shu Hashimoto, Yasuhiro Gon, Ken Matsumoto, Shuichiro Maruoka, Ikuko Takeshita, Shinichi Hayashi, Yasukiyo Asai, Yoshito Asai, Itsuro Jibiki, Tatsuya Machino and Takashi Horie
Journal of Pharmacology and Experimental Therapeutics May 2000, 293 (2) 370-375;
Shu Hashimoto
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Yasuhiro Gon
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Ken Matsumoto
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Shuichiro Maruoka
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Ikuko Takeshita
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Shinichi Hayashi
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Yasukiyo Asai
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Yoshito Asai
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Itsuro Jibiki
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Tatsuya Machino
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Takashi Horie
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Abstract

Adult respiratory distress syndrome (ARDS) characterized by permeability edema is observed in severe insults such as bacteremia sepsis. Interleukin (IL)-8, which chemoattracts and activates neutrophils, has been suggested to play an important role in the production of ARDS. Therefore, the inhibition of IL-8 production is an important strategy for the treatment of ARDS. Recent studies have revealed the role of p38 mitogen-activated protein (MAP) kinase in cytokine expression and the inhibition by a selective inhibitor of p38 MAP kinase activity of cytokine expression in a variety of cell types. However, little is known about the role of p38 MAP kinase in lipopolysaccharide (LPS)-induced IL-8 expression in pulmonary vascular endothelial cells and the effect of a selective p38 MAP kinase inhibitor on it. In the present study, we therefore attempted to clarify these issues. The results showed that LPS induced p38 MAP kinase phosphorylation and activity, and SB 203580 as a selective inhibitor of p38 MAP kinase activity inhibited p38 MAP kinase activity and IL-8 expression in LPS-stimulated pulmonary vascular endothelial cells. These results indicate that p38 MAP kinase regulates LPS-induced IL-8 expression in pulmonary vascular endothelial cells. Although it is currently not known whether SB 203580 is capable of producing beneficial effects on ARDS, a strategy of inhibiting p38 MAP kinase activity by a selective p38 MAP kinase inhibitor may apply to the therapy for ARDS.

Footnotes

  • Send reprint requests to: Dr. Shu Hashimoto, First Department of Internal Medicine, Nihon University School of Medicine, 30-1 Oyaguchikamimachi, Itabashi-Ku Tokyo 173-8610, Japan. E-mail:shuh{at}med.nihon-u.ac.jp

  • Abbreviations:
    ARDS
    adult respiratory distress syndrome
    IL
    interleukin
    LPS
    lipopolysaccharide
    MAP
    mitogen-activated protein
    HPAEC
    human pulmonary artery endothelial cell
    PAGE
    polyacrylamide gel electrophoresis
    ATF
    activating transcription factor
    • Received October 20, 1999.
    • Accepted December 23, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 293 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 293, Issue 2
1 May 2000
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Selective Inhibitor of p38 Mitogen-Activated Protein Kinase Inhibits Lipopolysaccharide-Induced Interleukin-8 Expression in Human Pulmonary Vascular Endothelial Cells

Shu Hashimoto, Yasuhiro Gon, Ken Matsumoto, Shuichiro Maruoka, Ikuko Takeshita, Shinichi Hayashi, Yasukiyo Asai, Yoshito Asai, Itsuro Jibiki, Tatsuya Machino and Takashi Horie
Journal of Pharmacology and Experimental Therapeutics May 1, 2000, 293 (2) 370-375;

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Selective Inhibitor of p38 Mitogen-Activated Protein Kinase Inhibits Lipopolysaccharide-Induced Interleukin-8 Expression in Human Pulmonary Vascular Endothelial Cells

Shu Hashimoto, Yasuhiro Gon, Ken Matsumoto, Shuichiro Maruoka, Ikuko Takeshita, Shinichi Hayashi, Yasukiyo Asai, Yoshito Asai, Itsuro Jibiki, Tatsuya Machino and Takashi Horie
Journal of Pharmacology and Experimental Therapeutics May 1, 2000, 293 (2) 370-375;
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