| 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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| 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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