c-Jun N-terminal Kinase Contributes to Norepinephrine-Induced Contraction Through Phosphorylation of Caldesmon in Rat Aortic Smooth Muscle

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著者

    • Lee Youn Ri LEE Youn Ri
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • KIM Hyojin
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • KIM Junghwan
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • KIM Jaeheung
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • LEE Keun Sang
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University
    • LEE Yun Lyul
    • Department of Physiology, College of Medicine, Hallym University
    • MIN Kyung Ok
    • Department of Physical Therapy, College of Natural Science, Yongin University
    • KIM Bokyung
    • Department of Physiology, College of Medicine, Institute of Biomedical Science and Technology, Konkuk University

抄録

Vascular smooth muscle contraction is mediated by activation of extracellular signal-regulated kinase (ERK) 1/2, an isoform of mitogen-activated protein kinase (MAPK). However, the role of stress-activated protein kinase/<i>c-Jun</i> N-terminal kinase (JNK) in vascular smooth muscle contraction has not been defined. We investigated the role of JNK in the contractile response to norepinephrine (NE) in rat aortic smooth muscle. NE evoked contraction in a dose-dependent manner, and this effect was inhibited by the JNK inhibitor SP600125. NE increased the phosphorylation of JNK, which was greater in aortic smooth muscle from hypertensive rats than from normotensive rats. NE-induced JNK phosphorylation was significantly inhibited by SP600125 and the conventional-type PKC (cPKC) inhibitor Gö6976, but not by the Rho kinase inhibitor Y27632 or the phosphatidylinositol 3-kinase inhibitor LY294002. Thymeleatoxin, a selective activator of cPKC, increased JNK phosphorylation, which was inhibited by Gö6976. SP600125 attenuated the phosphorylation of caldesmon, an actin-binding protein whose phosphorylation is increased by NE. These results show that JNK contributes to NE-mediated contraction through phosphorylation of caldesmon in rat aortic smooth muscle, and that this effect is regulated by the PKC pathway, especially cPKC.<br>

収録刊行物

  • Journal of pharmacological sciences  

    Journal of pharmacological sciences 100(2), 119-125, 2006-02-20 

    The Japanese Pharmacological Society

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各種コード

  • NII論文ID(NAID)
    10018240677
  • NII書誌ID(NCID)
    AA11806667
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13478613
  • NDL 記事登録ID
    7821821
  • NDL 雑誌分類
    ZS51(科学技術--薬学)
  • NDL 請求記号
    Z53-D199
  • データ提供元
    CJP書誌  CJP引用  NDL  J-STAGE 
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