| Project/Area Number |
18590058
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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 |
Biological pharmacy
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| Research Institution | Hiroshima International University |
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Principal Investigator |
IDE Toshinori Hiroshima International University, Faculty of Pharmaceutical Sciences, Professor (60012746)
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| Co-Investigator(Kenkyū-buntansha) |
MAEDA Shizuko Hiroshima International University, Faculty of Pharmaceutical Sciences, Research Associate (80435065)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | stem cells / hTERT / telomerase / telomere / cell life-span / immortal cells / celllar senescence / 細胞不死化 / 血管内皮細胞 / ヒト培養細胞 / 肝実質細胞 / 間葉系幹細胞 / ヒト細胞 |
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| Research Abstract |
Stem cells have three prominent characteristics, i.e., telomerase activity, unlimited proliferative life-span and ability to differentiate. Telomerase is an enzyme that elongates telomere sequences at each chromosome end and allows cells to proliferate indefinitely. Several lines of fragmental evidence, however, suggest that telomerase has additional roles for the maintenance of characteristics seen in stem cells. Premature senescence of cultured human fibroblasts was induced by continuous treatment with low concentrations of hydrogen peroxide, which was not observed in hTERT (human telomerase gene)-introduced fibroblasts under the same condition. To have some idea on the role of telomerase on the bypass of premature senescence, we searched for possible differences on signal transduction process during cell response between normal fibroblasts and hTERT-introduced fibroblasts and between cellular senescence and premature senescence. Enhancement of p21 was observed according to the progression of both cellular senescence and premature senescence of human fibroblasts, which was confirmed by reporter assay using p21 promoter conjugated by reporter gene. Enhancement of p21 was weak, if not at all, in hTERT-introduced cells which bypassed cellular senescence and premature senescence. We could not find the reason why hTERT-expressing fibroblasts bypassed premature senescence under which normal fibroblasts ceased proliferation.
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