Possible involvement of CaィイD12+ィエD1-signaling transferred to mitochondria in release of ATP as an autacoid

CaD12+D1 信号可能参与转移至线粒体并作为自体物质释放 ATP

基本信息

  • 批准号:
    10670102
  • 负责人:
  • 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 Scientific Research (C)
  • 财政年份:
    1998
  • 资助国家:
    日本
  • 起止时间:
    1998 至 1999
  • 项目状态:
    已结题

项目摘要

ATP is extracellularly released as an autocine/paracrine and served as a functional modulator via stimulating P2-receotors of cell types.Hitherto, however, it remains unprovided evidence for the release mechanism and intracellular source of ATP. The research project was planed to clarify the existence of CaィイD12+ィエD1-signal pathway from endoplasmic reticulum (ER) to mitochondria in the release for ATP. In 1998, we demonstrated in ideal longitudinal smooth muscles of guinea-pigs that the release of ATP evoked by stimulating P2Y-purioceptors with α, β-methylene ATP (α, β-mATP) resulted from increase of Ins(1, 4, 5)PィイD23ィエD2 production via activation of phospholipase C and subsequently, from enhanced release of CaィイD12+ィエD1 from CaィイD12+ィエD1 storage sites. From the study during 1999 carried out with the vas deferens smooth muscles, it has been considered the possibility that α, β-mATP stimulates P2X-purinodeptors and, then activates ryanodine receptors on endoplasmic reticulum (ER), like caffeine, and the subsequent release of CaィイD12+ィエD1 from ER generating the release of ATP. The evoked release of ATP seen in both smooth muscles was interfered with mitochondrial inhibitors such as rotenone. Accordingly, it is suggested that release of ATP couples with CaィイD12+ィエD1-signal pathways from ER to mitochondria. The viewpoint will be clarified in a further analysis using fluorescent CaィイD12+ィエD1-probes to measure [CaィイD12+ィエD1]i in cultured rat hepatocytes without contractility.
ATP在细胞外以自分泌/旁分泌的形式释放,并通过刺激不同类型细胞的P2受体而发挥功能调节剂的作用,但ATP的释放机制和胞内来源尚不清楚。本课题旨在阐明在ATP释放过程中是否存在从内质网(endoplasmic reticulum,ER)到线粒体的Ca ~(2+)-D_12 + D_1-信号通路。1998年,我们在豚鼠的理想纵行平滑肌中证明,用α,β-亚甲基ATP(α,β-mATP)刺激P2 Y-嘌呤受体(purioceptor)引起的ATP释放是由于通过激活磷脂酶C增加Ins(1,4,5)P β D23 β D2的产生,随后是由于Ca β D12+ Ca β D1储存位点的Ca β D12 + Ca β D1的释放增加。从1999年对输精管平滑肌进行的研究中,人们认为α,β-mATP可能刺激P2 X-嘌呤受体,然后激活内质网(ER)上的兰尼碱受体(如咖啡因),随后从ER释放Ca ~(2+)D12+ Ca ~(2+)D1,从而产生ATP的释放。在两种平滑肌中观察到的ATP的诱发释放受到线粒体抑制剂如鱼藤酮的干扰。因此,提示ATP的释放与从ER到线粒体的Ca ~(2+)D_12 + Ca ~(2+)D_1-信号通路偶联。这一观点将在使用荧光Ca ~(2+)D_1-探针测量培养的无收缩性大鼠肝细胞中[Ca ~(2+)D_1]i的进一步分析中阐明。

项目成果

期刊论文数量(22)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
T. Katsuragi et al.: "ATP release and inositol(1, 4, 5)trisphosphate accumulation induced by angiotensin II and tachykinin in intact and cultured guinea pig taenia coli"Naunyn-Schmiedeb. Arch. Pharmacol.. (in press).
T. Katsuragi 等人:“血管紧张素 II 和速激肽在完整和培养的豚鼠大肠杆菌中诱导 ATP 释放和肌醇 (1, 4, 5) 三磷酸积累”Naunyn-Schmiedeb。
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    0
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T. Katsuragi et al.: "The first international conference in control and diseases of dependent transportation proteins and ion channels."Elsevier Science B. V., The Netherlands. (in press).
T. Katsuragi 等人:“关于依赖运输蛋白和离子通道的控制和疾病的第一届国际会议。”Elsevier Science B. V.,荷兰。
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    0
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C.Sato et al.: "Cross desenstization on contractions by P2-agonists of guinea pig ileum"Jpn.J.Pharmacol.. 80. 311-317 (1999)
C.Sato 等人:“豚鼠回肠 P2 激动剂对收缩的交叉脱敏”Jpn.J.Pharmacol.. 80. 311-317 (1999)
  • DOI:
  • 发表时间:
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    0
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K. Shibata et al.: "Possible involvement of central C-type natriuretic polypeptide receptor on water intake in spontaneous hypertensive rats"Neuropeptides. (in press).
K. Shibata 等人:“中枢 C 型利尿钠多肽受体可能参与自发性高血压大鼠的水摄入”神经肽。
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  • 发表时间:
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  • 影响因子:
    0
  • 作者:
  • 通讯作者:
I. Makino et al.: "The increase in angiotensin type-2 receptor mRNA level by glutamate stimulation in cultured rat cortical cells"Brain Res.. 804. 296-305 (1998)
I. Makino 等人:“在培养的大鼠皮质细胞中通过谷氨酸刺激增加血管紧张素 2 型受体 mRNA 水平”Brain Res.. 804. 296-305 (1998)
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    0
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KATSURAGI Takeshi其他文献

KATSURAGI Takeshi的其他文献

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{{ truncateString('KATSURAGI Takeshi', 18)}}的其他基金

Identification of a specific transporter on extracellular release of ATP
细胞外释放 ATP 的特定转运蛋白的鉴定
  • 批准号:
    17590234
  • 财政年份:
    2005
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Involvement of a transporter in an autocrine / paracrine release of ATP.
转运蛋白参与 ATP 的自分泌/旁分泌释放。
  • 批准号:
    15590243
  • 财政年份:
    2003
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
ATP-autocrine/paracrine release and its intracellular Ca^<2+> signals
ATP-自分泌/旁分泌释放及其胞内Ca^2信号
  • 批准号:
    13670107
  • 财政年份:
    2001
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Intracellular signalling pathway involved in ATP release from isolated smooth muscle cells.
细胞内信号通路参与分离的平滑肌细胞释放 ATP。
  • 批准号:
    07670127
  • 财政年份:
    1995
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Involvement of ATP released from non-neuronal tlssues in presynaptic neuromodulation.
非神经元组织释放的 ATP 参与突触前神经调节。
  • 批准号:
    04670132
  • 财政年份:
    1992
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
A possible role as a neuromodulator of extraneuronally released-ATP.
可能作为神经元外释放的 ATP 的神经调节剂。
  • 批准号:
    02670102
  • 财政年份:
    1990
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
Novel characteristics of ATP as a potential neuro-co-transmitter.
ATP 作为潜在神经递质的新特征。
  • 批准号:
    61570114
  • 财政年份:
    1986
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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A novel approach to study mechanisms of age-related dysfunction in hypoxia-induced erythrocyte ATP release
一种研究缺氧引起的红细胞 ATP 释放中年龄相关功能障碍机制的新方法
  • 批准号:
    10707876
  • 财政年份:
    2022
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一种研究缺氧引起的红细胞 ATP 释放中年龄相关功能障碍机制的新方法
  • 批准号:
    10354521
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    2022
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Pannexin-1/P2X7 interaction promotes excessive ATP release in kidney cysts and ADPKD progression via reduced NaCl reabsorption
Pannexin-1/P2X7 相互作用通过减少 NaCl 重吸收促进肾囊肿中 ATP 过度释放和 ADPKD 进展
  • 批准号:
    10614647
  • 财政年份:
    2021
  • 资助金额:
    $ 1.34万
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Pannexin-1/P2X7 interaction promotes excessive ATP release in kidney cysts and ADPKD progression via reduced NaCl reabsorption
Pannexin-1/P2X7 相互作用通过减少 NaCl 重吸收促进肾囊肿中 ATP 过度释放和 ADPKD 进展
  • 批准号:
    10415031
  • 财政年份:
    2021
  • 资助金额:
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Investigation of compression-induced ATP release in head and neck carcinoma
头颈癌中压迫诱导的 ATP 释放的研究
  • 批准号:
    19K10019
  • 财政年份:
    2019
  • 资助金额:
    $ 1.34万
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神经元 ATP 释放机制分析
  • 批准号:
    539844-2019
  • 财政年份:
    2019
  • 资助金额:
    $ 1.34万
  • 项目类别:
    University Undergraduate Student Research Awards
Underlying mechanisms controlling urothelial ATP release and their contributions to urinary bladder physiology and pathophysiology
控制尿路上皮 ATP 释放的潜在机制及其对膀胱生理学和病理生理学的贡献
  • 批准号:
    10416026
  • 财政年份:
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Mechanisms of ATP-release in Cancer Cells
癌细胞中 ATP 释放的机制
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  • 资助金额:
    $ 1.34万
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    Grant-in-Aid for Scientific Research (C)
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控制尿路上皮 ATP 释放的潜在机制及其对膀胱生理学和病理生理学的贡献
  • 批准号:
    9767138
  • 财政年份:
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  • 资助金额:
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老年人红细胞 ATP 释放受损的机制和治疗
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  • 资助金额:
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