| Project/Area Number |
24591377
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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 |
Hematology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
IKUTA Katsuya 旭川医科大学, 医学部, 講師 (00396376)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Katsunori 旭川医科大学, 医学部, 特任教授 (60336394)
ITO Satoshi 旭川医科大学, 医学部, 特任助教 (80548686)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 非トランスフェリン結合鉄 / 鉄過剰症 / 造血障害 / 糖代謝異常 / 糖代謝 |
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| Outline of Final Research Achievements |
The present study was performed to elucidate the machanisms for the inhibition of hematopoiesis by iron overload and its recovery by iron chelation. Mice were administrated with iron dextran, and these mice showed iron deposition in bone marrow, increased serum iron and serum ferritin, and non-transferrin-bound iron (NTBI). Iron chelation therapy was also performed for those iron-overloaded mice. Comparison of gene expressions between those models indicated that the expressions of the genes related to glucose metabolism were changed responding to iron status. Among them, the expessions of aconitase and isocitrate dehedrogenase, those were important in TCA cycle, increased in iron overload and improved by iron chelation. 2-hydroxyglutarate (2-HG)and DNA methylation were also increased. Combinding our data, iron overload can increase DNA methylation via increase of 2-HG even without any mutation in IDH gene, finally resulting in the inhibition of hematopoiesis or leukemic change.
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