Information control for a linkage between macro cardiac function and gene expression: physiomic analysis of responses to oxygen environment
| Project/Area Number |
26282127
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biomedical engineering/Biomaterial science and engineering
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| Research Institution | Kawasaki Medical School |
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Principal Investigator |
Mohri Satoshi 川崎医科大学, 医学部, 教授 (00294413)
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| Co-Investigator(Kenkyū-buntansha) |
片野坂 友紀 岡山大学, 医歯(薬)学総合研究科, 助教 (60432639)
橋本 謙 川崎医科大学, 医学部, 講師 (80341080)
氏原 嘉洋 川崎医科大学, 医学部, 助教 (80610021)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2016: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Keywords | 細胞分裂 / 胎児酸素環境 / 心筋細胞 / 胎児循環 / 分裂促進因子 / 心筋肥大 / 後期促進複合体 / 分裂 / 酸素 / 細胞周期 / 再生医療 / 酸素環境 / 心筋 / エネルギー代謝 / 心筋分裂 / ユビキチン / プロテアソーム / 周産期 / 心臓メカニクス / カルシウム / 力学的環境 |
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| Outline of Final Research Achievements |
It is important to investigate the mechanisms of cell division and the regulation of energy consumption of cardiomyocyte for cardiovascular medicine. We identified Fam64a as an novel essential molecule for caudiomyocyte division. Fam64a was abundantly expressed in hypoxic fetal cardiomyocyte nuclei, but was sharply repressed by oxygen exposure, and also in postnatal cardiomyocytes. Fam64a knockdown inhibited and its overexpression enhanced the proliferation of cardiomyocytes. Non-degradable Fam64a mutant suggested that its optimum expression and subsequent degradation by anaphase-promoting complex/cyclosome before anaphase are required for cell division. Moreover, we revealed that short term triiodothyronine(T3) administration increased SERCA2 expression and decreased NCX1 expression but did not change cardiac contractility, resulting in energy-saving oxygen consumption for excitation-contraction coupling. Long term T3 administration decreased cardiac contractility and NCX activity.
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Report
(4 results)
Research Products
(33 results)
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[Journal Article] ANGPTL2 activity in cardiac pathologies accelerates heart failure by perturbing cardiac function and energy metabolism.2016
Author(s)
Tian Z, Miyata K, Kadomatsu T, Horiguchi H, Fukushima H, Tohyama S, Ujihara Y, Okumura T, Yamaguchi S, Zhao J, Endo M, Morinaga J, Sato M, Sugizaki T, Zhu S, Terada K, Sakaguchi H, Komohara Y, Takeya M, Takeda N, Araki K, Manabe I, Fukuda K, Otsu K, Wada J, Murohara T, Mohri S, Yamashita JK, Sano M, Oike Y.
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Journal Title
Nature Communications
Volume: 7
Issue: 1
Pages: 13016-13016
DOI
NAID
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Cdk5rap1-mediated 2-methylthio modification of mitochondrial tRNAs governs protein translation and contributes to myopathy in mice and humans.2015
Author(s)
Wei FY, Zhou B, Suzuki T, Miyata K, Ujihara Y, Horiguchi H, Takahashi N, Xie P, Michiue H, Fujimura A, Kaitsuka T, Matsui H, Koga Y, Mohri S, Suzuki T, Oike Y, Tomizawa K.
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Journal Title
Cell Metab
Volume: 21
Issue: 3
Pages: 413-6
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] TRPV2 is critical for the maintenance of cardiac structure and function in mice.2014
Author(s)
Katanosaka Y, Iwasaki K, Ujihara Y, Takatsu S, Nishitsuji K, Kanagawa M, Sudo A, Toda T, Katanosaka K, Mohri S, Naruse K.
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Journal Title
Nat Comm
Volume: 5
Issue: 1
Pages: 3932-3932
DOI
NAID
Related Report
Peer Reviewed / Open Access
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