Physiomic analyses of cardiac hypertrophy and ventricular geometry of in cardiac regulation
Project/Area Number |
23300171
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Biomedical engineering/Biological material science
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Research Institution | Kawasaki Medical School |
Principal Investigator |
MOHRI Satoshi 川崎医科大学, 医学部, 教授 (00294413)
|
Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Ken 川崎医科大学, 医学部, 講師 (80341080)
UJIHARA Yoshihiro 川崎医科大学, 医学部, 助教 (80610021)
宮坂 武寛 姫路獨協大学, 公私立大学の部局等, 教授 (60308195)
|
Co-Investigator(Renkei-kenkyūsha) |
NARUSE Keiji 岡山大学, 医歯(薬)学総合研究科, 教授 (40252233)
|
Project Period (FY) |
2011-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2013: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2011: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
|
Keywords | 心機能 / 心肥大 / 心筋分裂 / 酸素環境 / 機械受容 / 冠循環 / フィジオーム / カルシウム / 心不全 |
Research Abstract |
Cardiac pump function is determined by the quantity and quality of myocardium and ventricular geometry. We investigated the regulatory mechanism of the heart for the change in environment. First, we focused the effects of the change in oxygen tension on the cellular switching from division to hypertrophy during perinatal period. Fetal cardiomyocytes were harvested and cultured at different oxygen tension (low O2: 3%, high O2: 20%) . We firstly succeeded to visualize the division of cardiomyocytes using time-lapse motion picture under low O2 condition. Then, we found that cardiomyocytes stopped cell division under high O2 while they kept dividing under low O2 condition. We also performed micro-allay analysis to reveal the genes regulating cell cycle, which would be useful to make the adult cardiomyocytes to restart cell devision. As for the mechan-osensing in the heart, we show that TRPV2 cation channel is critical for the maintenance of cardiac structure and function.
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Report
(4 results)
Research Products
(15 results)
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[Journal Article] TRPV2 is critical for the maintenance of cardiac structure and function in mice2014
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 Commun
Volume: 5
Pages: 3932-3932
NAID
Related Report
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[Journal Article] TRPV2 is critical for the maintenance of cardiac structure and function in mice2014
Author(s)
Yuki katanosaka, Keiichiro Iwasaki, Yoshihiro Ujihara, Satomi Takatsu, Koki Nishitsuji, Motoi Kanagawa, Atsushi Sudo, Tatsushi Toda, Kimiaki Katanosaka, Satoshi Mohri, and Keiji Naruse
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Journal Title
Nature Communications
Volume: 未定
NAID
Related Report
Peer Reviewed
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