| Project/Area Number |
12670793
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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 |
Pediatrics
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| Research Institution | HYOGO COLLEGE OF MEDICINE |
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Principal Investigator |
YAMAMOTO Masuji Hyogo College of Medicine,Department of Pediatrics,Associate Professor, 医学部, 助教授 (40200844)
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| Co-Investigator(Kenkyū-buntansha) |
辻野 吉昭 兵庫医科大学, 医学部, 助手 (60268547)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cell cycle / MDS (myedysplastic syndrome) / TGF-b |
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| Research Abstract |
The effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor-bl (TGF-bl) on cell cycle regulation of SKM-1 myelodysplastic syndrome (MDS) cells was analysed. Our results indicated that TGF-bl-mediated Gl arrest correlated with the downregulation of cdk4, cdk6 and cyclin D2, and that abrogation of TGF-bl-mediated Gl arrest by GM-CSF was caused by the constitutive overexpression of cyclin D2 and cdk6 but not cdk4.The relationship between the cell surface antigen and the cell cycle regulation of human bone marrow hematopoietic progenitor cells was further analysed. Our results suggested that the cell cycle arrest of human bone marrow hematopoietic progenitor cells by TGF-b was associated with stage-specific expression of c-kit and CD38.These phenomenon may shed light on the etiology of hatatopoietic disorder, such as MDS.
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