Anti-inflammatory Properties of Cytochrome P450 Epoxygenase-Derived Eicosanoids

  • Koichi Node
    Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.
  • Yuqing Huo
    Department of Biomedical Engineering, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.
  • Xiulu Ruan
    Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.
  • Baichun Yang
    Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA.
  • Martin Spiecker
    Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.
  • Klaus Ley
    Department of Biomedical Engineering, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA.
  • Darryl C. Zeldin
    Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA.
  • James K. Liao
    Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, LMRC-322, Boston, MA 02115, USA.

抄録

<jats:p>The epoxyeicosatrienoic acids (EETs) are products of cytochrome P450 epoxygenases that have vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor. The cytochrome P450 isoform CYP2J2 was cloned and identified as a potential source of EETs in human endothelial cells. Physiological concentrations of EETs or overexpression of CYP2J2 decreased cytokine-induced endothelial cell adhesion molecule expression, and EETs prevented leukocyte adhesion to the vascular wall by a mechanism involving inhibition of transcription factor NF-κB and IκB kinase. The inhibitory effects of EETs were independent of their membrane-hyperpolarizing effects, suggesting that these molecules play an important nonvasodilatory role in vascular inflammation.</jats:p>

収録刊行物

  • Science

    Science 285 (5431), 1276-1279, 1999-08-20

    American Association for the Advancement of Science (AAAS)

被引用文献 (28)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ