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ELECTROPHARMACOLOGYCAL ANALYSIS OF INTRACELLULAR SIGNALTRANSDUCTIONS OF VASCULAR ENDOTHERIAL CELLS

ELECTROPHARMACOLOGYCAL ANALYSIS OF INTRACELLULAR SIGNALTRANSDUCTIONS OF VASCULAR ENDOTHERIAL CELLS
血管内皮细胞胞内信号传导的电药理学分析
批准号:
06670098
负责人:
IIJIMA Toshihiko
金额:
$1.34万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1994
资助国家:
日本
项目状态:
已结题
起止时间:
1994 至 1995

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项目成果

IIJIMA Toshihiko的其他基金

相关文献

中文摘要
翻译
在培养的血管内皮细胞中,组胺和三磷酸腺苷在高浓度(>10um)时产生一过性的细胞内游离钙离子浓度的持续升高。在本实验中,我们用钙荧光指示剂Fura-2在培养的人主动脉内皮细胞中研究了后者持续升高的机制。后者可通过去除胞外钙离子而消除,并可通过将胞外氯离子浓度降至40 mM或用氯离子通道阻断剂N-苯基邻氨基苯甲酸(NPA,1 mM)可逆地消除。同时观察内质网钙离子的特异性阻断剂thapsigargin和环哌酸(CPA)对[Ca^<2>-ATPase]_i的影响。山茶素(1-1000 nM)和CPA(0.1-100微米)引起[Ca^<2>]_i的双相变化。缓慢下降的阶段被细胞外钙的去除消除,并被低氯条件和NPA阻止。这些结果表明,组胺、ATP、thapsigarin和CPA引起的[Ca^<2>]_i的持续升高是由于[Ca^<2>2>_i和/或通过耗尽培养的人主动脉内皮细胞内的钙储备。
英文摘要
In cultured vascular endothelial cells, histamine and ATP at high concentrations (>10 muM) produce an initial transient followed by sustained elevation in intracellular free Ca^<2+> concentration ([Ca^<2+>]_i). In the present experiments, mechanisms responsible for the latter sustained elevation were studied in cultured human aortic endothelial cells loaded with the fluorescent Ca^<2+> indicator fura-2. The latter phase was eliminated by removal of extracellular Ca^<2+>, and was reversibly abolished by reduction of extracellular Cl^- concentration to 40 mM or by the Cl^- channel blocker N-phenylanthranilic acid (NPA,1 mM). Effects of thapsigargin and cyclopiazonic acid (CPA), specific inhibitors of endoplasmic reticulum Ca^<2+>-ATPase, on [Ca^<2+>]_i were also examined. Thapsigargin (1-1000 nM) and CPA (0.1-100 muM) produced a biphasic change in [Ca^<2+>]_i. The slow declining phase was eliminated by removal of extracellular Ca^<2+> and was prevented by the low Cl^- condition and NPA.These results suggest that the sustained elevation of [Ca^<2+>]_i in response to histamine, ATP,thapsigargin and CPA is produced by the Cl^--sensitive entry of extracellular Ca^<2+> activated by the rise in [Ca^<2+>]_i and/or by the depletion of intracellular Ca^<2+> stores in cultured human aortic endothelial cells.
期刊论文(10)
专著(0)
科研奖励(0)
会议论文
E.Hosoki & T.Iijima: "Modulation of cytosolic Ca^<2+> concentration by thapsigargin and cyclopiazonic acid in human aortic endothelial cells." Eur. J. Pharmacol. (Mol. Pharmacol. Sec.). 288. 131‐137 (1995)
E.Hosoki 和 T.Iijima:“毒胡萝卜素和环吡嗪酸对人主动脉内皮细胞中胞质 Ca^2+ 浓度的调节”。Eur. J. Pharmacol. 288. 131‐。 137 (1995)
DOI: --
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期刊:
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作者: []
通讯作者:
Molecularpharmacological analysis of mechanosensitive cation channels in vascular endothelial cells.
  • 批准号:
    18590230
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.57万
  • 财政年份:
    2006
  • 负责人:
    IIJIMA Toshihiko
  • 依托单位:
Molecularpharmacological analysis of mechanosensitive cation channels in vascular endothelial cells.
  • 批准号:
    16590189
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.18万
  • 财政年份:
    2004
  • 负责人:
    IIJIMA Toshihiko
  • 依托单位:
Molecular Pharmacology of Capacitative Ca^<2+> Entry Channel of Human Aortic Endothelial Cell
  • 批准号:
    12670080
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.5万
  • 财政年份:
    2000
  • 负责人:
    IIJIMA Toshihiko
  • 依托单位:
Molecular and Electropharmacological Analysis of Capacitative Ca^<2+> Entry channels of Vascular Endothelial Cells
  • 批准号:
    09670087
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 资助金额:
    $2.05万
  • 财政年份:
    1997
  • 负责人:
    IIJIMA Toshihiko
  • 依托单位: