| Project/Area Number |
09671379
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Tottori University |
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Principal Investigator |
KURODA Hiroaki Tottori University, Faculty of Medicine, Assistant Professor, 医学部, 助教授 (70186550)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUDA Naruto Tottori University, Faculty of Medicine, Assistant, 医学部, 助手 (30291462)
ISHIGURO Shingo Tottori University, Faculty of Medicine, Assistant Professor, 医学部・附属病院, 講師 (70212868)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | PKC / ischemia-reperfusion / isolated cardiomyocyte / CaィイD12+ィエD1 / AnィイD1+ィエD1-CaィイD12+ィエD1 exchange / intracellular pH / ischemic preconditioning / 蛋白燐酸化酵素C / 虚血再潅流 / Ca^<2+>過負荷 / 細胞長 / 筋小胞体 |
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| Research Abstract |
The aims of this study were to test the effects of protein kinase C (PKC) activation on the intracellular CaィイD12+ィエD1 concentration of rat cardiomyocytes during chemical hypoxia-reoxygenation ; to determine the contribution of the sarcoplasmic reticulum (SR) and the AnィイD1+ィエD1-CaィイD12+ィエD1 exchange on the regulation of intracellular CaィイD12+ィエD1 following PKC activation, and to test the role of PKC-dependent intracellular pH changes in intracellular CaィイD12+ィエD1 regulation. We used the isolated adult rat cardiomyocyte perfusion model. Cardiomyocytes were loaded with the CaィイD12+ィエD1-fluorescent probe Fluo-3 and the pH-fluorescent probe SNARF1. Cells were subjected to 50 minutes of glucose-free and NaCN chemical hypoxia followed by 30 minutes of simulated reoxygenation. The activation of PKC significantly inhibited the hypoxia-induced increase of Fluo-3 fluorescent intensity. This inhibitory effect was not affected by the inhibition of the SR CaィイD12+ィエD1 uptake, but was cancelled by the inhibition of the AnィイD1+ィエD1-CaィイD12+ィエD1 exchange. PKC activation also attenuated the decrease in intracellular pH during chemical hypoxia. We concluded that the PKC attenuation of CaィイD12+ィエD1 overloading to rat cardiomyocytes during chemical hypoxia-reoxygenation does not depend on the CaィイD12+ィエD1 uptake by the SR, but does require AnィイD1+ィエD1-CaィイD12+ィエD1 exchange. Since PKC attenuated the increasing intracellular HィイD1+ィエD1 during chemical hypoxia, a low HィイD1+ィエD1 concentration may be important for the maintenance of CaィイD12+ィエD1 extrusion via the AnィイD1+ィエD1-CaィイD12+ィエD1 exchange.
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