| Project/Area Number |
10670713
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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 |
Pediatrics
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| Research Institution | Fukui Medical University |
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Principal Investigator |
TSUKAHARA Hirokazu Faculty of Medicine, Fukui Medical University, Assistant, 医学部, 助手 (90207340)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | nitric oxide / endothelin / vascular endothelium / bone metabolism / metabolic bone disease / redox / ラット / 骨組織 / 微小血管内皮細胞 |
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| Research Abstract |
The following is the summary of my current research project.
1. Role of endothelin/endothelin receptor subtype A system in the control of bone metabolism (Reference #3)
We found that the long-term blockade of the endothelin A receptor reduces bone formation and induces osteopenia in growing rats. This result suggests that endothelin produced by vascular endothelial cells plays an important role in bone growth and metabolism in vivo.
2. Redox modulation of vascular endothelial cell function (Reference #4. 6, 7)
Using the electrical cell-substrate impedance sensor technique, we observed that nitric oxide (NO) modulates cell-matrix and/or cell-cell adhesion in human microvascular endothelial cells and suggested that NO might modify microvascular permeability in humans. We also found the importance of the constitutive NO synthase activity in the maintenance of oxidant buffering capacity in rats.
3. Pathophysiology of endothelial cell dysfunction (Reference #5)
We have summarized our recent observations implicating insufficient NO production in pathological states (e.g., atherosclerosis, hypertension and heart failure) in the inappropriate response to angiogenic stimuli.
4. Assessment of bone metabolism in infantile metabolic bone diseases
We demonstrated for the first time that the low bone turnover state lies in the infantile osteopenia imperfecta type3.
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