Ontogenetic and phylogenetic mechanisms involved in the loss of proliferation activity in mammalian cardiomyocytes after birth.
| Project/Area Number |
24650245
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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 |
Biomedical engineering/Biological material science
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 心筋細胞増殖 / イモリ心筋 / ラット心筋 / 正帰還制御ループ / 心筋損傷後再生 / 心筋細胞増殖能喪失 |
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| Research Abstract |
Shortly after birth, mammalian cardiomyocytes irreversibly exit from the cell cycle and become terminally differentiated. In contrast, a newt’s heart can be completely repaired and the organ’s function can be completely restored following damage. The genetic cues for the irreversible exit from the cell cycle in mammalian cardiomyocytes soon after birth remain largely unknown. This study aims at elucidating ontogenetic and phylogenetic mechanisms involved in the loss of proliferation activity in mammalian cardiomyocytes soon after birth. To investigate the causes underling the lack of proliferation activity in mammalian cardiomyocytes, I examined the effect of an extract derived from newt regenerating hearts on terminally differentiated rat cardiomyocytes. This study has demonstrated that the exposure of rat cardiomyocytes to the protein extract derived from newt regenerating hearts resulted in an increase in the proliferation activity of rat cardiomyocytes, suggesting that the unknown protein(s) involved in the newt extract possibly opened a positive-feedback loop of ROS-p38 MAPK-Cx43 contributing to the loss of proliferation activity in mammalian cardiomyocytes.
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Report
(2 results)
Research Products
(6 results)
