| Project/Area Number |
26293045
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | National Institute for Physiological Sciences (2017)
The Graduate University for Advanced Studies (2014-2016) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
岡田 俊昭 生理学研究所, 生体機能調節研究領域, 特任准教授 (00373283)
松浦 博 滋賀医科大学, 医学部, 教授 (60238962)
沼田 かお理 (佐藤かお理 / 沼田 かお理(佐藤かお理)) 生理学研究所, 大学共同利用機関等の部局等, 研究員 (60614196)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
Fiscal Year 2016: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2015: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | アニオンチャネル / 心臓 / ATP放出 / 虚血・再灌流 / 左心室発生圧 / アニオンチャンネル |
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| Outline of Final Research Achievements |
Cellular release of ATP is a key event in purinergic signaling in animal tissues. We showed previously that the ATP release is mediated by Maxi-Cl in many cell types including cardiomyocytes. Here, we have identified SLCO2A1, which is known to be a prostaglandin transporter (PGT), as the pore component of Maxi-Cl. Also, we have shown that SLCO2A1 is involved in swelling-induced ATP release from Maxi-Cl-rich C127 cells. When Langendorff-perfused mouse hearts were subjected to oxygen-glucose deprivation (OGD), ATP was released to the coronary effluent upon reperfusion. This OGD-induced heart ATP release was suppressed by in vivo pre-injection of SLCO2A1-siRNA or by application of a PGT blocker, indicating a SLCO2A1 involvement in the OGD-induced cardiac ATP release. This ATP release was associated with increased left ventricular developed pressure, in a manner sensitive to an adenosine A1 receptor antagonist, suggesting a protective role of released ATP via A1 receptor signaling.
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