| Project/Area Number |
26501007
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Regenerative medicine
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| Research Institution | Kindai University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MORIYAMA Mariko 近畿大学, 薬学総合研究所, 客員准教授 (40595295)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 間葉系幹細胞 / 分化能 / Notchシグナル / 解糖系 / 代謝 / 低酸素 |
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| Outline of Final Research Achievements |
Human adipose tissue-derived multilineage progenitor cells (hADMPCs) are attractive for cell therapy and
tissue engineering because of their multipotency and ease of isolation without serial ethical issues. Here, we show that Notch signaling is required for glycolysis regulation under hypoxic conditions. Our results demonstrate that 5% O2 dramatically increased the glycolysis rate, improved the proliferation efficiency, prevented senescence, and maintained the multi potency of hADMPCs. Hypoxia significantly increased the level of activated Notch1 and expression of its downstream gene, HES1. Furthermore, Hypoxia markedly increased glucose consumption and lactate production, which decreased back to normoxic levels on treatment with a g-secretase inhibitor. We also found that HES1 was involved in induction of GLUT3, TPI, and PGK1 in addition to reduction of TIGAR and SCO2 expression. These results clearly suggest that Notch signaling regulates glycolysis under hypoxic conditions.
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