Laminar Shear Stress Up-Regulates Inducible Nitric Oxide Synthase in the Endothelium

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著者

    • OZAWA Naoko
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School
    • SHICHIRI Masayoshi
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School
    • IWASHINA Masatora
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School
    • FUKAI Nozomi
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School
    • YOSHIMOTO Takanobu
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School
    • HIRATA Yukio
    • Department of Clinical and Molecular Endocrinology, Tokyo Medical and Dental University Graduate School

抄録

<B>Shear stress caused by blood flow is a potent physiological stimulus for the generation of nitric oxide (NO) in endothelial cells, which is believed to derive from the up-regulation and post-transcriptional activation of endothelial constitutive NO synthase (ecNOS). However, it has yet to be demonstrated that inducible NO synthase (iNOS) plays a significant role in shear stress-induced NO production from endothelial cells. We used parallel plate-type flow chambers that detect fluid shear stress to determine that shear stress, as quantified by a real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR), increased iNOS gene transcripts in cultured endothelial cells, which resulted in increased NO production. Shear stress-induced iNOS expression was inhibited by pyrrolidine dithiocarbamate (PDTC), an antioxidant and nuclear factor κB (NF-κB) blocker, and by MG132, an aldehyde peptide proteasome inhibitor that antagonizes IκB-kinase. Laminar shear stress increased the transcriptional activity of NF-κB, whereas over-expression of an IκB-α mutant that inhibits the activation of NF-κB in a dominant-negative fashion was found to attenuate the induction of endothelial iNOS by shear stress. The present results demonstrate that shear stress induces iNOS in the endothelium, mainly <I>via</I> the activation of NF-κB. (<I>Hypertens Res</I> 2004; 27: 93-99)</B>

収録刊行物

  • Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension

    Hypertension research : clinical and experimental : official journal of the Japanese Society of Hypertension 27(2), 93-99, 2004-02-01

    The Japanese Society of Hypertension

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各種コード

  • NII論文ID(NAID)
    10012843557
  • NII書誌ID(NCID)
    AA10847079
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    09169636
  • データ提供元
    CJP書誌  J-STAGE 
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