| Project/Area Number |
01480354
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kyoto University |
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Principal Investigator |
KIKUCHI H Kyoto Univ., Fac. of Medicine, Prof., 医学部, 教授 (20072746)
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| Co-Investigator(Kenkyū-buntansha) |
HOSHIMARU M Kyoto Univ., Fac. of Medicine, Ass. Prof., 医学部, 助手 (70211539)
NAGATA I Kyoto Univ., Fac. of Medicine, Ass. Prof., 医学部, 講師 (10198327)
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| Project Period (FY) |
1989 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | moyamoya disease / spontaneous occlusion of the circle of Willis / bFGF / FGF receptor / FLG / superficial temporal artery / bFGFリセプタ- / 免疫組織化学 / 単純ヘルペスウィルス / 硬膜 / DNAブロット解析 / aFGF |
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| Research Abstract |
The primary lesion of moyamoya disease is stenosis of the intracanial arterial trunk, which is thought to result in extensive collateral circulation, including a fine network of vessels at the base of the brain. However, the cause of moyamoya disease remains unknown, and pathophysiological mechanisms remain unproven. Basic fibroblast growth factor (BFGF) is a potent mitogen for a number of cell types including vascular endothelial and smooth muscle cells. In order to test the possibility that BFGF takes part in the pathogenesis of the intimal thickening of moyamoya disease, we tested for the presence of BFGF using a mouse anti-human BFGF monoclonal antibody. We demonstrated immunohistochemically that the amount of BFGF is increased in the superficial temporal artery (STA) of patients with moyamoya disease. Then, we performed an immunohistochemical study of STA using a polyclonal anti-human FGF receptor (FLG) antibody to clarify the function of BFGF. This study demonstrated that BFGF coexists with BFGF receptor in smooth muscle cells. Thus, we speculate that smooth muscle cells with abundant BFGF may stimulate themselves through an autocrine mechanism and migrate into the intima and then thicken it. Although we performed DNA blot analyses to examine a change in the BFGF and BFGF receptor gene, we could not find out the major change in the BFGF and BFGF receptor gene of patients with moyamoya disease. In addition, we have performed polymerase chain reaction (PCR) to detect herpes simplex virus (HSV) genomes in patients with moyamoya disease. However, HSV genomes are present in both normal adults and patients with moyamoya disease in a high frequency. We have failed to elucidate the cause of the increased production of BFGF. Further examination is required to reveal the cause of the increased production of BFGF.
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