Studies on molecular mechanisms of thalidomide-induced teratogenesis using human mesenchymal tem cells
| Project/Area Number |
19510076
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | National Institute of Health Sciences |
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Principal Investigator |
TAKAGI Atsuya National Institute of Health Sciences, 毒性部, 室長 (00179417)
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| Project Period (FY) |
2007 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | サリドマイド / 間葉系幹細胞 / マイクロアレイ / 遺伝子 / ヒト / マウス / 発生・分化 |
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| Research Abstract |
There are many proposed mechanisms of action in thalidomide teratogenicity including inhibition of angiogenesis or oxidative DNA damage. We have undertaken a microarray gene expression analysis on human mesenchymal stem cells and mouse mesenchymal stem like cells treated with thalidomide. No clear changes of gene expression including oxidative stress were observed (10μM thalidomide) in the human cells. On the other hand, dose-dependent decrease of a long non-coding RNA was observed in mouse mesenchymal stem like cells (10-300μM thalidomide).
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Report
(4 results)
Research Products
(5 results)
