Proton signaling mediated by voltagegated proton channels

由电压门控质子通道介导的质子信号传导

基本信息

  • 批准号:
    14570045
  • 负责人:
  • 金额:
    $ 2.18万
  • 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:
    2002
  • 资助国家:
    日本
  • 起止时间:
    2002 至 2003
  • 项目状态:
    已结题

项目摘要

We have investigated how the voltage-gated proton (H^+) channels regulate H^+ signaling in osteoclasts, microglia and bone-marrow-derived mast cells (BMMC). The Q_<10> value was > 2.0 for conductance and 3 -6 for gating parameters. These high Q_<10> values were preserved well in both microglia and BMMC, which differed in the expression rate of the channel, implying that the high temperature dependence resides in the channel itself. The Q_<10> value for the conductance was, however, often decreased at high temperature or in swollen cells, thus, indicating that the activation status of the H^+ channel is heterogeneous. To clarify actions of the H^+ channel in intact cells, the channel activity in response to various types of cell acidosis was examined in the perforated-whole cell recordings under intrinsic pH buffers. In osteoclasts, an activator for protein kinase C, PMA, induced cell acidosis and activation of the H^+ channel. The reversal potential was served as a real-time monitor for changes in cellular pH in clamped cells. In microglia, the H^+ channel was activated accompanying either acute or prolonged cell acidosis. The channel activation terminated upon removal of the acidosis due to the H^+ extrusion. A part of the activation was, however, modified by ΔpH-independent processes. In addition, sometimes increases in intracellular Ca^<2+> or flux of CL^-, a counter ion for H^+, were associated with the acidosis. Thus H^+ signaling is intimately related to synergistic actions of other ion signals. This study has provided evidences that the H^+ can maintain cellular pH homeostasis by sensing minor changes in pH disturbances and, simultaneously, would trigger H^+ to the surrounding cells.
我们研究了电压门控质子(H^+)通道如何调节破骨细胞、小胶质细胞和骨髓源性肥大细胞(BMMC)中的H^+信号。电导的Q_<10>值&gt; 2.0,门控参数的Q_值为3 - 6。这些高Q<10>值在小胶质细胞和BMMC中均得到很好的保持,这表明通道的高温度依赖性存在于通道本身。然而<10>,电导的Q值在高温或肿胀的细胞中经常降低,因此,表明H^+通道的激活状态是不均匀的。为了阐明H^+通道在完整细胞中的作用,我们在内源性pH缓冲液中,通过穿孔全细胞记录,检测了响应于各种类型细胞酸中毒的通道活性。在破骨细胞中,蛋白激酶C激活剂PMA可诱导细胞酸中毒和H^+通道激活。逆转电位作为一个实时监测细胞pH值的变化,在夹紧的细胞。在小胶质细胞中,H^+通道被激活,伴随着急性或长期的细胞酸中毒。由于H^+排出,酸中毒消除后,通道激活终止。然而,一部分活化被Δ pH非依赖性过程修饰。此外,有时细胞内Ca^2+或CL^-(H^+的抗衡离子)流量的增加也与酸中毒有关。因此,H^+信号与其他离子信号的协同作用密切相关。本研究提供的证据表明,H^+可以通过感知pH扰动的微小变化来维持细胞内pH的稳态,同时也会将H^+触发到周围的细胞。

项目成果

期刊论文数量(58)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
森泰生, 稲垣千代子, 久野みゆき, 井上隆司, 岡田泰伸, 今泉祐治: "薬理学のQOLへの貢献2:細胞増殖・分化・死を制御するイオンメカニズムと創薬"Folia Pharmacol.Jpn.. 122. 201-214 (2003)
Yasuo Mori、Chiyoko Inagaki、Miyuki Kuno、Takashi Inoue、Yasunobu Okada、Yuji Imaizumi:“药理学对 QOL 2 的贡献:控制细胞增殖、分化和死亡的离子机制和药物发现” Folia Pharmacol.Jpn.. 122 .201 -214 (2003)
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Morihata, H., Mori, H., Sakai, H., Kawawaki, J., sawada, M., Tsutada, T., Kuno, M.: "Activation of voltage-gated proton channels and calcium mobilization upon acute and prolonged cell acidosis in rat micorogilia"Biophys.J.. 86. 129a (2004)
Morihata, H.、Mori, H.、Sakai, H.、Kawawaki, J.、sawada, M.、Tsutada, T.、Kuno, M.:“电压门控质子通道的激活和急性和长时间的钙动员
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Shimakawa, S., Suzuki, S., Miyamoto, R., Takitani, K., Tanaka, K., Tanabe, T., Wakamiya, E., Nakamura, F., Kuno, M., Matsuura, S., Watanabe, Y., Tamai, H.: "Neuropilin-2 is overexpresed in the rat brain after limbic seizures."Brain Res.. 956. 67-73 (2002)
岛川,S.,铃木,S.,宫本,R.,泷谷,K.,田中,K.,田边,T.,若宫,E.,中村,F.,久野,M.,松浦,S.,
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Mori, H., Sakai, H., Morihata, H., Yamano, T., Kuno, M.: "A voltage-gated H^+ channel is a powerful mechanism for pH homeostasis in murine steoclasts"Kobe J Med Sci. 48. 87-96 (2002)
Mori, H.、Sakai, H.、Morihata, H.、Yamano, T.、Kuno, M.:“电压门控 H^ 通道是小鼠破骨细胞 pH 稳态的强大机制”Kobe J Med Sci。
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Kuno, M., Morihata, H., Mori H., Kawawaki, J.: "Effects of temperature on the voltage-gated proton channels and proton signaling"Jpn.J.Physiol.. Vol.52,Suppl.. S117 (2002)
Kuno, M.、Morihata, H.、Mori H.、Kawawaki, J.:“温度对电压门控质子通道和质子信号传导的影响”Jpn.J.Physiol.. Vol.52,Suppl.. S117(
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KUNO Miyuki其他文献

KUNO Miyuki的其他文献

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{{ truncateString('KUNO Miyuki', 18)}}的其他基金

Functions of vacuolar H+-ATPases and voltage-gated proton channels coexisted in the plasma membrane of osteoclasts
破骨细胞质膜中液泡H-ATP酶和电压门控质子通道的功能共存
  • 批准号:
    23390043
  • 财政年份:
    2011
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Temperature-sensitive recruitment of voltage-gated proton channels
电压门控质子通道的温度敏感募集
  • 批准号:
    20590213
  • 财政年份:
    2008
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Roles of proton channels in proton signaling : pH-clamp and analysis of proton current oscillation
质子通道在质子信号传导中的作用:pH钳和质子电流振荡分析
  • 批准号:
    16590168
  • 财政年份:
    2004
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Regulatory mechanisms of activity and expression of voltage-gated proton channels
电压门控质子通道的活性和表达的调节机制
  • 批准号:
    12670045
  • 财政年份:
    2000
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
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
  • 财政年份:
    1998
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Ion channels and the regulatory mechanisms in different phenotypic mast cells derived from bone marrow hematopoietic stem cells
骨髓造血干细胞不同表型肥大细胞的离子通道及调控机制
  • 批准号:
    05670052
  • 财政年份:
    1993
  • 资助金额:
    $ 2.18万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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