| Project/Area Number |
26670189
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Experimental pathology
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| Research Institution | Mie University |
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Principal Investigator |
Hashizume Ryotaro 三重大学, 医学(系)研究科(研究院), 助教 (50456662)
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| Co-Investigator(Kenkyū-buntansha) |
Shimojo Naoshi 藤田保健衛生大学, 医学部, 客員講師 (70410751)
Takanari Hiroki 大分大学, 医学部, 助教 (70723253)
Kuroda Taruho 三重大学, 医学系研究科, 助教 (00391946)
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| Co-Investigator(Renkei-kenkyūsha) |
Hara Mari 三重大学, 医学部, 教務職員 (30176383)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 心筋再生 / 細胞質分裂 / 二核化 / プロテオミクス / 細胞周期 / 細胞分裂 |
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| Outline of Final Research Achievements |
Cardiomyocytes dramatically proliferate in fetal life, however, exit the cell cycle soon in the perinatal period in mammals. In this process, DNA synthesis takes place in the absence of cytokinesis, resulting in bi-nucleation of the myocytes. Our proteome analysis identified more than 12 proteins relevant to cytokinesis of a rat ventricular myocyte. In the cell culture system with cells isolated from a rat neonate ventricle, we found that activation of ECT2 does not govern cardiomyocyte cell fate, in which myocytes undergo whether nuclear mitosis coupled with cytokinesis or acytokinetic mitosis. Furthermore, the study revealed that the cell fate of the neonatal cardiomyocyte is fairly dependent upon PLK1 expression, known as an early trigger for G2/M transition, which imply the cell fate has been already determined at an early period in the cell cycle. Finally, deconstruction of the cellular sarcomere structure was shown to be non-specific phenomenon to cytokinesis of the myocyte.
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