| Project/Area Number |
25460393
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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 |
Pathological medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAGO KENJI 自治医科大学, 医学部, 講師 (20306111)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ST2 / IL-33 / 線維芽細胞 / 細胞増殖 / NIH-3T3 cells / シグナル伝達 / 分泌 / ST2L / NIH-3T3 / 抗がん作用 |
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| Outline of Final Research Achievements |
The ST2 gene was originally identified as a gene induced during the initiation of cell proliferation. Since the products had a sequence very similar to the interleukin 1 receptor and IL-33 was found as a ligand inducing inflammatory responses, the major concern has been immunological aspect. In the present study, coming back to the original findings, we investigated the roles of IL-33 and ST2 in cell proliferation of NIH-3T3 fibroblastic cell line. IL-33 had dual functions, namely, a suppressive effect on the growth initiation of quiescent cells, and a growth-promoting effect on cycling cells. On the other hand, contrary to the initial hypothesis, soluble ST2 had a growth-promoting effect.
The relationship between IL-33 and ST2 in terms of growth regulation remains to be elucidated in future.
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