EXPERIMENTAL STUDY ON GLIAL RESPONSES TO NEONATAL HYPOXIC/ISCHEMIC ENCEPHALOPATYH
| Project/Area Number |
06670785
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
OHNO Masaki SHIGA UNIVERSITY OF MEDICAL SCIENCE,DEPARTMENT OF PEDIATRICS,ASSISTANT, 医学部, 助手 (50194254)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | HYPOXIC / ISCHEMIC / ENCEPHALOPATHY / NEONATE / GLIA / MICROGLIA / PDGF / アストログリア / 神経栄養因子 |
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| Research Abstract |
In the first year of the research project, we have investigated the cellular responses to hypoxic/ischemic encephalopathy in the neonatal rats. Left common carotid artery of the 7-day-old rats was ligated, and the pups were placed in a hypoxic chamber. The glial responses were examined using the immunocytochemistry. The results indicate that developing microglia are the first and principle glial element that responds to hypoxic/ischemic injury during the neonatal period. The astrocyte respose occurs later. These glial responses may play important roles in the neuronal degeneration and/or tissue remodeling.
In the second year of the research project, expressions of platelet-derived growth factor (PDGF) B-chain and PDGF beta-receptor have been investigated in the immature brains with hypoxic/ischemic injury. The expressions of PDGF B-chain and its specific receptor protein and mRNA were examined using an immunocytochemistry and a northern analysis, respcetively. The results indicate that neonatal hypoxic/ischemic insult induces the upregulation of PDGF B-chain and beta-receptor expressions in neurons immediately after hypoxia. This upregulation, however, was tentative in most neurons. Sublethal damage on neurons in peri-infarct areas induces the sustained and long-term upregulations of PDGF B-chain and beta-receptor. PDGF B-chain molecules may act as a neuroprotective factor in developing brain with hypoxic/ischemic injury through autocrine and paracrine mechanisms.
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Report
(3 results)
Research Products
(21 results)
