The role of mechanosensor molecule TRPV2 during monocyte transmigration across vascular endothelium in atherogenesis.
Project/Area Number |
25350544
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Biomedical engineering/Biomaterial science and engineering
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Research Institution | Kawasaki Medical School |
Principal Investigator |
Hashimoto Ken 川崎医科大学, 医学部, 講師 (80341080)
|
Co-Investigator(Kenkyū-buntansha) |
Mohri Satoshi 川崎医科大学, 医学部, 教授 (00294413)
Ujihara Yoshihiro 川崎医科大学, 医学部, 助教 (80610021)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 動脈硬化 / 血管内皮細胞 / 単球 / 浸潤 / TRPV2 / メカノセンサー / 内皮細胞 / 細胞骨格 / 細胞周期 |
Outline of Final Research Achievements |
Adhesion and subsequent transmigration of blood monocytes across vascular endothelial cells are critical in early atherogenesis. We focused on the physical and mechanical interaction of monocytes and endothelial cells, and examined the role of TRPV2, Ca2+-permeable mechanosensor molecule expressed in endothelial cells. Biochemical analysis including TRPV2 knockdown and overexpression system revealed that TRPV2 is an essential molecule for cell survival by promoting cell migration and proliferation. It promotes cell migration by facilitating pseudopodium formation at the cell membrane through regulating actin cytoskeleton. The role of TRPV2 in the context of monocyte-endothelial interaction during transmigration is the subject of future study.
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Report
(4 results)
Research Products
(13 results)
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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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[Journal Article] Increased Passive Stiffness of Cardiomyocytes in the Transverse Direction and Residual Actin and Myosin Cross-Bridge Formation in Hypertrophied Rat Hearts Induced by Chronic β-Adrenergic Stimulation2013
Author(s)
Sumita Yoshikawa W, Nakamura K, Miura D, Shimizu J, Hashimoto K, Kataoka N, Toyota H, Okuyama H, Miyoshi T, Morita H, Fukushima Kusano K, Matsuo T, Takaki M, Kajiya F, Yagi N, Ohe T, Ito H.
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Journal Title
Circulation Journal
Volume: 77
Issue: 3
Pages: 741-748
DOI
NAID
ISSN
1346-9843, 1347-4820
Related Report
Peer Reviewed
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