Role of neuronal calcium sensor-1 as a cardioprotective factor and its possible mechanism.
| Project/Area Number |
24590293
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | 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 Cardiovascular Center Research Institute |
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Principal Investigator |
NISHITANI Tomoe 独立行政法人国立循環器病研究センター, 研究所, 室長 (50393244)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Ca2+シグナル / 心筋 / サバイバル / ミトコンドリア / 酸化ストレス / 虚血―再灌流 / カルシウムセンサー / 心臓 / イノシトールリン酸 / カルシウムシグナル |
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| Outline of Final Research Achievements |
Identifying molecular targets that regulate cardiomyocyte survival is of therapeutic importance for conquering heart failure. Neuronal Ca2+-sensor-1 (NCS-1) is an EF-hand Ca2+-binding protein, which is important for excitable cell functions. Our preliminary results suggest that NCS-1 is involved in stress tolerance in the heart, therefore we examined this hypothesis. We found that NCS-1 deficient (KO) mouse hearts were more susceptible to oxidative (H2O2) and metabolic stress, as well as ischemia-reperfusion injury. Cellular ATP levels, mitochondrial respiration rates (basal and maximal O2 consumption, and proton leak), and activation of Akt survival pathways were significantly depressed in KO myocytes; especially with oxidative stress. These results suggest that NCS-1 plays an important role in mitochondrial detoxification system and hence regulates cardiac survival under stress.
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Report
(4 results)
Research Products
(40 results)
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[Journal Article] Deficiency of a lipid droplet protein, perilipin 5, suppresses myocardial lipid accumulation, thereby preventing type 1 diabetes-induced heart malfunction.2014
Author(s)
3.Kuramoto K, Sakai F, Yoshinori N, Nakamura TY, Wakabayashi S, Kojidani T, Haraguchi T, Hirose F, Osumi T.
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Journal Title
Mol. Cell. Biol.
Volume: 34
Pages: 2721-31
Related Report
Peer Reviewed / Acknowledgement Compliant
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[Journal Article] Defect of a lipid droplet protein, Perilipin 5, prevents diabetes-induced heart malfunction by suppressing lipid accumulation.2014
Author(s)
Kuramoto K, Sakai F, Yoshinori N, Nakamura TY, Wakabayashi S, Kojidani T, Haraguchi T, Hirose F, Osumi T.
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Journal Title
Mol. Cell Biol.
Volume: in press
Related Report
Peer Reviewed
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[Presentation] Infant Sudden Death: Novel Mutations Responsible for Impaired Nav1.5 Channel Function.2015
Author(s)
Morganstein, J., Jana, K., Foster, M.N., Nakamura, T.Y., McDonald, T.V., Tang, Y., Coetzee, W.A.
Organizer
Biophysical Society 59th Annual Meeting
Place of Presentation
Baltimore/USA
Year and Date
2015-02-07 – 2015-02-11
Related Report
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