| Project/Area Number |
62570544
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Kyoto University |
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Principal Investigator |
SAWADA Hiroyoshi The Faculty of Medicine, Kyoto University, 医学部, 講師 (30093248)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | HL-60 cell / K-562 cell / Differentiation / dbcAMP / Staurosporine / Lysozyme mRNA / 蛋白合成 / dbcAMP / H8 / OAG / Staurosporine / HL-60細胞 / K-562細胞 / 1α25(OH)_2D_3 / Retinoic Acid / Caイオン / Mgイオン / スタウロスポリン / 細胞内シグナル伝達 |
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| Research Abstract |
The role of second messengers on differentiation of HL-60 cells and K-562 cells was investigated. HL-60 cell differentiation induced by various compounds except TPA was enhanced by dbcAMP, an activator of protein kinase A, and staurosporine, an inhibitor of protein kinase C. On the other hand OAG, an activator of protein kinase C, enhanced K-562 cell differentiation into erythrocyte lineage induced by hemin. However OAG did not enhance K-562 cell differentiation induced by other agents such as Ara-C, and actinomycin-D.
Expression of lysozyme mRNA was investigated in the process of HL-60 cell differentiation. Northern blot analysis revealed that lysozyme mRNA was expressed as cell differentiation progressed, and this expression was completely inhibited by cycloheximide, suggesting new protein synthesis is essential before differentiation related phenotypes are expressed.
Present results indicate that both activation of second messengers and new protein synthesis are necessary for the signal transduction from a commitment step to a phenotype expression step in leukemic cell differentiation.
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