The role of Notch3 receptor on destruction of the vascular smooth muscle cells in the brain arteries.
| Project/Area Number |
15590920
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology (2004)
National Center of Neurology and Psychiatry (2003) |
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Principal Investigator |
TAKAHASHI Keikichi National Institute for Longevity Sciences, National Center for Geriatrics and Gerontology, Department of vascular dementia research, (研究所)・血管性痴呆研究部, 部長 (40117148)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Notch3 / CADASIL / Vascular smooth muscle cells / Vascular dementia / Signal transduction / Jagged / Microarray analysis / Calcium channel / 血管性痴呆 / シグナル受容体 / 血管平滑筋 / 白質脳症 |
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| Research Abstract |
Mutations in the Notch3 receptor are associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy(CADASIL). Brains of patients affected by CADASIL show degeneration of vascular smooth muscle cells(SMC) and the abnormal accumulation of the extracellular domain(ECD) of Notch3. However, the mechanisms underlying pathological alterations in CADASIL are unclear.
In the present study, we determined specific genes which were regulated in vascular smooth muscle cells by Notch3. By the DNA array analysis, we found three genes. TARA-like protein gene and calcium channel were induced by the treatment of ligands, while DUSP23 were decreased. These genes may relate to proliferation and differentiation of vascular smooth muscle cells.
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Report
(3 results)
Research Products
(4 results)
