| Project/Area Number |
21790902
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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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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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 血液内科学 / 鉄代謝 / ヘプシジン / トランスフェリン受容体2 / 肝細胞 / トランスフェリン / siRNA / NTBI(非トランスフェリン結合鉄) / functional assay / atomic force microscopy |
|---|
| Research Abstract |
At first I demonstrated the characteristics of binding to transferrin and iron uptake of transferrin receptor 2 (TfR2) compared to 1 (TfR1). Then, I tried to establish the stable cell lines that overexpress TfR2 or HFE, and the stable cell lines in that TfR2 or HFE expression was suppressed by knockdown. The changes of the expression levels of those were determined by RT-PCR or western blot. Next, the effects of the changes of Tf-Fe_2 concentration in cell culture medium on hepcidin expressions in hepatoma-derived cells were determined, but I did not observe any significant change against my expectation. However, I focused on the possibility that non-hepatocyte might have function to sensor iron status, and found that monocyte-derived cell line might have that.
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