| Project/Area Number |
13670084
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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 |
General pharmacology
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| Research Institution | GIFU UNIVERSITY |
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Principal Investigator |
NIWA Masayuki Gifu University, School of Medicine, Associate Professor, 医学部, 助教授 (40156146)
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| Co-Investigator(Kenkyū-buntansha) |
KOZAWA Osamu Gifu University, School of Medicine, Professor, 医学部, 教授 (90225417)
MATSUNO Hiroyuki Gifu University, School of Medicine, Associate Professor, 医学部, 助教授 (40273148)
植松 俊彦 岐阜大学, 医学部, 教授 (50151832)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | plasminogen activator / neural damage / excitotoxin / transient ischemia / apoptosis / NMDA / retina / TUNEL method / 神経細胞死 / 線溶系 / 遺伝子制御 |
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| Research Abstract |
To investigate the role of tissue plasminogen activator (tPA) in retina, we compared neuronal damage in the retina in tPA deficient, tPA(-/-), mice and their wild type. Retinal damage was induced by intravitreal injection of excitotoxins, N-methyl-D-malainimide(NMDA) and kainic acid (KA), and by transient ischemic insult produced by elevating intraocular pressure. TdT-dUTP terminal nick-end labeling (TUNEL) method was used to examine the retinal damage. Number of NMDA-induced TUNEL positive cells in retina of tPA(-/-) mice was significantly smaller than those of wild type. In contrast, KA-induced and transient ischemic insult-induced TUNEL positive cells in retina from both types of mice showed no difference with significance. These results strongly indicated that tPA plays neuroprotective factor to protect retinal damage induced by excitotoxins, at least NMDA.
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