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Functional roles and regulatory mechanisms of voltage-gated proton channels

Functional roles and regulatory mechanisms of voltage-gated proton channels
电压门控质子通道的功能作用和调节机制
批准号:
10670047
负责人:
KUNO Miyuki
金额:
$1.73万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1998
资助国家:
日本
项目状态:
已结题
起止时间:
1998 至 1999

项目摘要

项目成果

KUNO Miyuki的其他基金

相关文献

中文摘要
翻译
电压-门控质子channels are unique mechanisms to exclude a massive amount of hy D1+ hy D1 from the inside of cells, and are considered to contributed to a rapid regulation of intracellular pH. We studed expression and regulatory mechanisms of the hy D1+ hy D1 currents in cells with different functions, such as, bone marrow-derived mast cells (BMMC),大鼠脊柱微胶质细胞和Murine osteoclasts。Recently high sensitivity to temperature has been found to be a common feature of H-D1 + H-D1 currents in many types of cells。在BMMC和微胶质细胞中,稳定状态电流、激活延迟和激活速率依赖于22和36℃之间温度的极大幅度。“半激活电压被转移到了更多的消极潜力,因为两个细胞都在加热。”当前激活的温度设定点在BMMC中可能高于其内在闸门属性或模块化机制。超过90%的圆形/淀粉样微球表达的H D ... More 1+爱D1 currents。H-D1 + H-D1 currents were increased in association with cell swelling induced by intracellular dialysis with acidic pipette solutions (pH 5.5-6.8)。acidosis-induced cell swelling and the accompanying potentiation of the Hy D1+ Hy D1 currents required non-hydrolytic actions of intracellular ATP and were inhibited by agents affecting actin filaments (phaloidin and cytochalasin D), as the hypotonically-activated Cly D1-Hy D1 channel in osteoclasts。These findings suggest that cell swelling induced by either intracellular acidification or osmotic imbalance is a crucial signal to increase the Hy D1+イエD1 currents of microglia。The swelling-mediated regulation of the Hy D1 channel might operate as a negative feedback Mechanism to protect microglia from cytotoxic acidification and swelling in the pathological CNS。These results suggest that activities of the HイD1+イエD1 channels are regulated in relation to their functional states and phenotypes and are involved in the various pathophysiolocal effen。Less(低)
英文摘要
Voltage-gated proton (HィイD1+ィエD1) channels are unique mechanisms to exclude a massive amount of HィイD1+ィエD1 from the inside of cells, and are considered to contribute to a rapid regulation of intracellular pH. We studied expression and regulatory mechanisms of the HィイD1+ィエD1 currents in cells with different functions, such as, bone marrow-derived mast cells (BMMC), rat spinal microglia and murine osteoclasts. Recently high sensitivity to temperature has been found to be a common feature of HィイD1+ィエD1 currents in many types of cells. In both BMMC and microglia, the amplitude of steady-state currents, the activation delay, and the activation rate depended greatly on temperature between 22 and 36℃. The half activation voltage was shifted to more negative potentials by heating in both cells. The temperature set-point for the current activation was higher in BMMC possibly due to its intrinsic gating properties or modulatory mechanisms. More than 90% of round/amoeboid microglia expressed HィイD … More 1+ィエD1 currents. The HィイD1+ィエD1 currents were increased in association with cell swelling induced by intracellular dialysis with acidic pipette solutions (pH 5.5-6.8). The acidosis-induced cell swelling and the accompanying potentiation of the HィイD1+ィエD1 currents required non-hydrolytic actions of intracellular ATP and were inhibited by agents affecting actin filaments (phalloidin and cytochalasin D), as the hypotonically-activated ClィイD1-ィエD1 channel in osteoclasts. These findings suggest that cell swelling induced by either intracellular acidification or osmotic imbalance is a crucial signal to increase the HィイD1+ィエD1 currents of microglia. The swelling-mediated regulation of the HィイD1+ィエD1 channel might operate as a negative feedback mechanism to protect microglia from cytotoxic acidification and swelling in the pathological CNS. These results suggest that activities of the HィイD1+ィエD1 channels are regulated in relation to their functional states and phenotypes and are involved in the various pathophysiolocal effects. Less
期刊论文(24)
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会议论文
Sakai, H. et al.: "Synergetic activation of outwardly rectifying Cl^- currents by hypotonic stress and external Ca^<2+> in murine osteoclasts"J. physiol. 515. 157-168 (1999)
Sakai,H.等人:“在小鼠破骨细胞中通过低渗应激和外部Ca ^ 2 协同激活向外整流的Cl ^ -电流”J。
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通讯作者:
Sakai, H. et al.: "Co-operative action of hypotonic stress and a rise in external Ca^<2+> on Cl^- currnets of murine osteoclasts"Excerpta Medica Internation, Congress Series. (in press).
Sakai,H.等人:“低渗应激和外部Ca ^ 2 增加对小鼠破骨细胞Cl 2 -电流的协同作用”国际医学摘录,国会系列。
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久野みゆき 他: "膜電位依存性プロトン(H^+)チャネルの温度依存性の解析" 第76回生理学会大会. 発表予定.
Miyuki Kuno 等人:“膜电位门控质子 (H^+) 通道的温度依赖性分析”第 76 届日本生理学会大会演讲。
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通讯作者:
Kuno, M. et al.: "Behaviors of voltage-gated proton channels at different temperature in mast cells and microglia"Biophysical j. (Abstract). 78. 2072 (2000)
Kuno, M. 等人:“肥大细胞和小胶质细胞中不同温度下电压门控质子通道的行为”Biophysical j。
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共 24 条
    Functions of vacuolar H+-ATPases and voltage-gated proton channels coexisted in the plasma membrane of osteoclasts
    • 批准号:
      23390043
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $5.08万
    • 财政年份:
      2011
    • 负责人:
      KUNO Miyuki
    • 依托单位:
    Temperature-sensitive recruitment of voltage-gated proton channels
    • 批准号:
      20590213
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.0万
    • 财政年份:
      2008
    • 负责人:
      KUNO Miyuki
    • 依托单位:
    Roles of proton channels in proton signaling : pH-clamp and analysis of proton current oscillation
    • 批准号:
      16590168
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.24万
    • 财政年份:
      2004
    • 负责人:
      KUNO Miyuki
    • 依托单位:
    Proton signaling mediated by voltagegated proton channels
    • 批准号:
      14570045
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.18万
    • 财政年份:
      2002
    • 负责人:
      KUNO Miyuki
    • 依托单位: