| Project/Area Number |
26293021
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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 |
Pharmacology in pharmacy
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| Research Institution | Nagoya City University |
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Principal Investigator |
Imaizumi Yuji 名古屋市立大学, 大学院薬学研究科, 教授 (60117794)
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| Co-Investigator(Kenkyū-buntansha) |
山村 寿男 名古屋市立大学, 大学院薬学研究科, 准教授 (80398362)
鈴木 良明 名古屋市立大学, 大学院薬学研究科, 助教 (80707555)
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| Co-Investigator(Renkei-kenkyūsha) |
Higuchi Tsunehiko 名古屋市立大学, 薬学研究科, 教授 (50173159)
Asai Kiyofumi 名古屋市立大学, 医学研究科, 教授 (70212462)
Hirono Syuichi 北里大学, 薬学部, 教授 (30146328)
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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 |
¥16,770,000 (Direct Cost: ¥12,900,000、Indirect Cost: ¥3,870,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2014: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
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| Keywords | イオンチャネル / 薬理学 / 薬学 / カルシウムシグナル / 創薬 / 蛍光イメージング / パッチクランプ / 生理学 / 生体分子 / シグナル伝達 / イメージング / 生物物理 / カルシウムシグナリング / ストア作動性カルシウム流入 / 細胞膜電位 / Kir2.1チャネル / ClC-7チャネル / CRACチャネル / 脳血管内皮細胞 / 軟骨細胞 |
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| Outline of Final Research Achievements |
The present study revealed that in non-excitable cells such as chondrocytes andendothelial cells, Ca2+-activated K+ (KCa) channels and store-operated Ca2+ (SOC) channels play significant roles in the positive feedback mechanism for the regulation of intracellular Ca2+ concentration ([Ca2+]i). This [Ca2+]i elevation forms cellular responses to various types of stimulations in physiological conditions or gets involved in pathological process. In chondrocytes, it is demonstrated that ion channels, such as large-conductance Ca2+-activated K+ (BK) channels, Ca2+-release-activated Ca2+ (CRAC) channels, ClC-3 and ClC-7, are involved in progression of osteoarthritis. In brain capillary endothelial cells, hypoxic stress induces the up-regulation of Kir2.1, augment of positive-feedback mechanisms and promotion of cell proliferation. These events may play a role in disruption of blood-brain-barrier after cerebral hypoxia.
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