| Project/Area Number |
08670918
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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 | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
TAKAHASHI Yuji Tokyo University of Pharmacy and Life Science, School of life Science, Associate Professor, 生命科学部, 助教授 (20154875)
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| Co-Investigator(Kenkyū-buntansha) |
MIURA Takashi Tokyo University of Pharmacy and Life Science, School of life Science, Professor, 生命科学部, 教授 (70013323)
TAKAHASHI Shigeru Tokyo University of Pharmacy and Life Science, School of life Science, Research, 生命科学部, 助手 (10266900)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | hypoxia / phosphoglycerate mutase B / differential display / fibroblast / prolyl 4-hydroxylase / rat / fetus |
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| Research Abstract |
Molecular oxygen (O2) is essential for aerobic organisms. Exposure of tissues or cells to hypoxia induces a variety of adaptive or pathogenic responses. To understand the mechanism and processes of cellular response to hypoxia, we exposed fetal rat lung fibroblasts to hypoxia (pO2=5Pa) and screened the hypoxia-responsible gene by the differential display method. Exposure of the cells to hypoxia activated the phosphoglycerate mutase B (PGM-B) and prolyl 4-hydroxylase (P4H) alpha gene, resulting in the induction of PGM enzymatic activity, concomitant with elevations of PGM-B mRNA and protein levels. The mRNA level was elevated linearly with decreases in partial O2 pressure, indicating a 2-3 fold increase in these levels after 16 h hypoxia. Up-regulation of PGM mRNA by hypoxia was obvious after 8 h exposure, reached its peak after 16 h, persists for 40 h and returned to the basal level after reoxygenation at 20% O2 for 16 h. Run-on and stability assays indicated that PGM-B expression is regulated mainly at the transcriptional step. These results suggest that the induction of PGM-B may contribute to the regulation of glycolytic flux under reduced O2 tension and play a role in the adaptation of cells to hypoxia.
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