| Project/Area Number |
23390020
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological 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, 薬学研究科(研究院), 教授 (60117794)
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| Co-Investigator(Kenkyū-buntansha) |
OHYA Susumu 京都薬科大学, 薬学部, 教授 (70275147)
YAMAMURA Hisao 名古屋市立大学, 薬学研究科, 准教授 (80398362)
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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) |
2011-11-18 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
Fiscal Year 2013: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
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| Keywords | 薬理学 / イオンチャネル / 非興奮性細胞 / カルシウム活性化カリウムチャネル / 正帰還カルシウム制御機構 / 細胞内カルシウム動態 / 発現調節 / ストア作動性カルシウムチャネル / 薬理 / ストア作動性カルシウム流入 / カリウムチャネル / カルシウムチャネル / イオンチャネル標的創薬 / ストア依存性カルシウム流入 / 分子イメージング |
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| Research Abstract |
The present study revealed that, in non-excitable cells such as endothelial cells, lymphocytes, chondrocytes and airway cilliated cell, 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 elicites cellular responses to various types of stimula under physiological conditions or is involved in pathological processes. In brain capillary endothelial cells and chondrocytes, Ca2+-release activated Ca2+ channel is a major component of SOC channels and regulates cell proliferation. In T lymphocytes isolated from inflammatory disease model mice, the change in expression level of intermediate-conductance KCa channel is related to pathological processes. In ciliated cells, ATP-sensitive K+ channel contribute to the positive feedback mechanism for [Ca2+]i, and facilitate ciliary movement and consequently promote airway clearance.
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