| Project/Area Number |
25670451
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | Osaka University |
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Principal Investigator |
KANAKURA YUZURU 大阪大学, 医学(系)研究科(研究院), 教授 (20177489)
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| Co-Investigator(Kenkyū-buntansha) |
ORITANI Kenji 大阪大学, 大学院医学系研究科, 准教授 (70324762)
ICHII Michiko 大阪大学, 大学院医学系研究科, 寄附講座助教 (30633010)
SAITOH Norimitsu 大阪大学, 大学院医学系研究科, 特任助教(常勤) (30597399)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 老化 / 造血幹細胞 / 分化 / Wnt / クロマチン / リンパ球 / SATB1 / sFRP5 / 内科 |
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| Outline of Final Research Achievements |
We established transgenic chimera mice to produce soluble Frizzled-related protein (sFRP)-5 under the immunoglobulin-kappa promoter. Overexpression of sFRP-5 inhibited B lymphocyte differentiation after the level of common lymphoid progenitors, leading to massive decrease of B lymphocytes in spleen. On the other hand, sFRP-5 deficient mice showed significant decrease of hematopoietic stem cells (HSC) when the mice were stimulated by estrogen. We established reporter mice, which monitor Special AT-rich sequence binding protein 1 (SATB1) gene expression. HSC contained two populations divided by SATB1-positivity, and the SATB1-positive cells had less HSC characters and more lymphocyte production than SATB1-negative cells.
Therefore, we successfully clarified in vivo roles of sFRP-5 and SATB1 in the lymphocyte production. Our results provide useful information to understand HSC aging.
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