Characterization and functional analyses of Hic-5 deficient mice
Project/Area Number |
20790076
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Biological pharmacy
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Research Institution | Showa University |
Principal Investigator |
KANEYAMA Shuri Showa University, 医学部・生化学, 講師 (10338535)
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Co-Investigator(Renkei-kenkyūsha) |
TAKEDA Naoki 熊本大学, 生命資源研究支援センター生物資源発研究部門技術開発分野, 助教 (90304998)
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Project Period (FY) |
2008 – 2009
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Project Status |
Completed (Fiscal Year 2009)
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Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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Keywords | Hic-5 / ノックアウトマウス / 動脈硬化 / 細胞接着 |
Research Abstract |
Hic-5(hydrogen peroxide-inducible clone-5) is a focal adhesion adaptor protein proposed as a candidate for a mediator of mechanotransduction. In the present study, we generated Hic-5-deficient mice by targeted mutation. Mice lacking Hic-5 are viable and fertile, and show no obvious histological abnormalities including vasculature. However, after wire injury of the femoral artery in Hic-5 deficient mice, histological recovery of arterial media was delayed due to enhanced apoptosis of vascular wall cells, whereas neointima formation was enhanced. Stretch-induced apoptosis was enhanced in cultured vascular smooth muscle cells from Hic-5 deficient mice.
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Report
(3 results)
Research Products
(7 results)
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[Journal Article] Hic-5, an adaptor protein expressed in vascular smooth muscle cells, modulates the arterial response to injury in vivo2008
Author(s)
Kim-Kaneyama JR M, Nose K., Wachi N, Sata M, Enomoto S, Fukabori K, Koh K, Shibanuma M, Nose K.
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Journal Title
Biochem Biophys Res Commun 376(4)
Pages: 682-7
Related Report
Peer Reviewed
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