Signal transduction mechanisms in negulation of Na/Ca exchanger via PI(4,5)P_2
通过 PI(4,5)P_2 调节 Na/Ca 交换器的信号转导机制
基本信息
- 批准号:14570039
- 负责人:
- 金额:$ 2.24万
- 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
- 来源:
- 关键词:
项目摘要
To investigate the regulatory mechanisms of Na^+-Ca^<2+> exchange under physiological conditions, we recorded Na^+-Ca^<2+> exchange current (I_<NaCa>) in the inside-out patch excised from guinea-pig ventricular myocytes (the macro patch). Applying ATP or PI(4,5)P_2 to the cytoplasmic surface of the patch membrane augmented the I_<NaCa>. Treatment of the patch membrane with PI-specific phospholipase C, which inhibits the production of PI(4,5)P_2 from PI, attenuated the ATP effect. This result suggests that the stimulatory effect of ATP is in part due to the production of PI(4,5)P_2 from PI. However, the application of inhibitors of protein tyrosine phosphatase, vanadate or bpV(phen), significantly augmented the I_<NaCa> in the presence of ATP. This result and others suggest that protein phosphorylation, probably protein tyrosine phosphorylation, is also involved in the stimulatory ATP effect on the I_<NaCa>.To validate the report that the PKA signaling stimulates the Na^+-Ca^<2+> activity, we measured whole-cell I_<NaCa> from guinea-pig ventricular myocytes. Isoproterenol, which is an agonist of the β-adrenoceptor, activated the cAMP-dependent Cl^-current, but did not stimulate the I_<NaCa>. We concluded that the PKA signaling does not stimulate the Na^+-Ca^<2+> exchange in guinea-pig ventricular cells. The previous reports might underestimate the activation of the cAMP-dependent Cl^-current.To study the regulatory mechanisms of NCX3, which is mainly expressed in brain and skeletal muscle, we measured the I_<NaCa> in the giant membrane patch excised from oocytes expressing NCX3. It was revealed that NCX3 possesses both the Ca^<2+>-dependent activation and inactivation, and that the increase of the I_<NaCa> by ATP is less potent in NCX3 than NCX1.
为了研究生理条件下Na^+-Ca^<2+>交换的调节机制,我们记录了豚鼠心室肌细胞内面朝外膜片(宏膜片)的Na^+-Ca^<2+>交换电流(I_<NaCa>)。将ATP或PI(4,5)P_2作用于膜片膜的胞质表面,可增加I_(10)<NaCa>。用PI特异性磷脂酶C处理膜片膜,可抑制PI产生PI(4,5)P_2,从而减弱ATP效应。这一结果表明,ATP的刺激作用部分是由于PI产生PI(4,5)P_2所致。然而,蛋白酪氨酸磷酸酶抑制剂钒酸盐或bpV(phen)的应用,显着增加了在ATP存在下的I_2<NaCa>。这一结果和其他结果表明,蛋白质磷酸化,可能是蛋白质酪氨酸磷酸化,也参与了ATP对I_2的刺激作用。<NaCa>为了验证PKA信号刺激Na^+-Ca^<2+>活性的报道,我们测量了<NaCa>豚鼠心室肌细胞的全细胞I_2。β-肾上腺素受体激动剂异丙肾上腺素激活cAMP依赖性Cl^-电流,但不刺激I_<NaCa>。我们的结论是PKA信号不刺激豚鼠心室肌细胞的Na^+-Ca^<2+>交换。为了研究主要在脑和骨骼肌中表达的NCX 3的调节机制,我们测量了<NaCa>从表达NCX 3的卵母细胞中切下的巨膜斑中的I_2。结果表明,NCX 3具有Ca^<2+>依赖的激活和失活作用,ATP对I_2的增加作用<NaCa>在NCX 3中弱于NCX 1。
项目成果
期刊论文数量(38)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Sarai N, Matsuoka S, Kuratomi S, Ono K, Noma A.: "Role of Individual Ionic Current Systems in the SA Node Hypothesized by a Model Study."Japanese Journal of Physiology. 53. 125-134
Sarai N、Matsuoka S、Kuratomi S、Ono K、Noma A.:“模型研究假设的个体离子电流系统在 SA 节点中的作用。”日本生理学杂志。
- DOI:
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- 影响因子:0
- 作者:
- 通讯作者:
松岡 達: "Na/Ca交換輸送体の構造と機能"心臓HEART. 34. 296-305 (2002)
T. Matsuoka:“Na/Ca 交换转运蛋白的结构和功能”Heart HEART 34. 296-305 (2002)
- DOI:
- 发表时间:
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- 影响因子:0
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Matsuoka S.: "Stoichiometry of the Na^+-Ca^<2+> exchanger : models & implications."Annals of the New York Academy of Sciences.. 976. 121-132 (2002)
Matsuoka S.:“Na^ -Ca^<2> 交换器的化学计量:模型
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- 影响因子:0
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Sarai N, Kihara Y, Izumi T, Mitsuiye T, Matsuoka S., Noma A.: "Nonuniformity of sarcomere shortenings in the isolated rat ventricular myocyte."Japanese Journal of Physiology. 52. 371-381 (2002)
Sarai N、Kihara Y、Izumi T、Mitsuiye T、Matsuoka S.、Noma A.:“离体大鼠心室肌细胞中肌节缩短的不均匀性。”日本生理学杂志。
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- 影响因子:0
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Powell T., Matsuoka S., Sarai N., Noma A.: "Intracellular Ca^<2+> dynamics and sarcomere length in ventricular myocytes."Cell Calcium.. 35. 535-542 (2004)
Powell T.、Matsuoka S.、Sarai N.、Noma A.:“心室肌细胞中的细胞内 Ca^<2> 动力学和肌节长度。”细胞钙.. 35. 535-542 (2004)
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MATSUOKA Satoshi其他文献
MATSUOKA Satoshi的其他文献
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{{ truncateString('MATSUOKA Satoshi', 18)}}的其他基金
Predicting the fate of lymphocytes by the initial Ca response pattern
通过初始 Ca 反应模式预测淋巴细胞的命运
- 批准号:
23650258 - 财政年份:2011
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Study on structure and function of mitochondria Na-Ca exchange(NCLX)
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23390042 - 财政年份:2011
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Studies on regulation of matrix ion dynamics and energy metabolism by mitochondria NCX
线粒体NCX对基质离子动力学和能量代谢的调控研究
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20390057 - 财政年份:2008
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Study of functional coupling among membrane excitation, contraction and mitochondria in cardiac myocyte.
心肌细胞膜兴奋、收缩与线粒体功能耦合研究。
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17590186 - 财政年份:2005
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Research on Peer-to-peer large-scale data processing on the Grid
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13224034 - 财政年份:2001
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research on Priority Areas
Wide-Area Grid Cluster for Parallel Optimization
用于并行优化的广域网格集群
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12480068 - 财政年份:2000
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Reconfigurable Parallel Processing Plug&Play Clustering
可重构并行处理即插即用集群
- 批准号:
12558025 - 财政年份:2000
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Study on ion transport of cardiac Na^+-K^+ pump and Na^+-Ca^<2+> exchnage
心脏Na^-K^泵离子转运及Na^-Ca^<2>交换的研究
- 批准号:
11670041 - 财政年份:1999
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Interactive Software Architecture for Advanced Movile Interface
高级移动界面的交互式软件架构
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10480055 - 财政年份:1998
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Function and molecular mechanism of Na^+-Ca^<2+> exchange
Na^-Ca^<2>交换的功能及分子机制
- 批准号:
09670043 - 财政年份:1997
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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