| Project/Area Number |
23390042
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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 |
General physiology
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| Research Institution | University of Fukui (2013)
Kyoto University (2011-2012) |
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Principal Investigator |
|
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| Co-Investigator(Kenkyū-buntansha) |
TAKEUCHI Ayako 福井大学, 医学部, 特命助教 (00378704)
|
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| Co-Investigator(Renkei-kenkyūsha) |
KIM Bongju 徳島大学, 疾患プロテオゲノム研究センター, 助教 (80511823)
|
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,760,000 (Direct Cost: ¥15,200,000、Indirect Cost: ¥4,560,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2011: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
|
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| Keywords | トランスポーター / ミトコンドリア / カルシウム / 心筋細胞 / リンパ球 / シミュレーション / Na-Ca交換 / 自動能 |
|---|
| Research Abstract |
In B lymphocyte cell lines (A20 and DT 40), it was demonstrated that mitochondrial Na/Ca exchanger (NCLX) is associated with mitochondrial Ca extrusion, modulation of endoplasmic reticulum Ca content, endoplasmic reticulum Ca release upon BCR-stimulation, store-operated Ca entry and chemotaxis. In cardiomyocyte cell line (HL-1), it was also demonstrated NCLX extrudes mitochondrial Ca and modulates sarcoplasmic reticulum Ca content. Additionally, it was found that NCLX modulates spontaneous beating frequency. These results were well reproduced by mathematical models of B lymphocyte, HL-1 cell and sinoatrial node cell. Taken together, it was suggested that NCLX act as a Ca provider from mitochondria to sarco- and endo-plasmic reticulum.
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