| Project/Area Number |
03671190
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
KUDO Jiro KYUSHU UNIVERSITY FAC.OF MED.Assistant Professor, 医学部, 助手 (90148940)
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| Co-Investigator(Kenkyū-buntansha) |
HIRATA Yasuhiko KYUSHU UNIVERSITY FAC.OF MED.Assistant Professor, 医学部, 助手 (10218787)
ISHIBASHI Hiromi KYUSHU UNIVERSITY FAC.OF MED.Lecturer, 医学部, 講師 (80127969)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | mitochondria / NADH dehydrogenase / leukemia / rotenone / inhibitor of mitochondria / cell cycle / cellular differentiation / HL-60 cells / アンチセンスオリゴヌクレチド / チトクロ-ムCオキシダ-ゼ / 細胞増殖 |
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| Research Abstract |
In a previous study,we elucidated that the mitochondrial NADH dehydrogenase subunit2(ND2)gene was overexpressed in human acute myelogenous leukemia(AML)cells as compared with normal granulocytes.Since the results of the study suggested that the ND2 gene expression depend on the maturation of HL-60 cells,the effect of rotenone,a specific NADH dehydrogenase inhibitor,and ND2 antisense DNA on cellular growth and differentiation of HL-60 cells has been investigated.Low dose of rotenone(50nM)inhibited the growth of HL-60 cells and rotenone-treated cells showed an increase of the cell population in the G_2+M phase.In regard to quantitative comparison of myeloid antigens,CD38 was relatively increased in rotenone-treated HL60 cells and rotenone-treated cells displayed upmodulation of CD13 in comparison with untreated cells.Expression of the ND2 gene in rotenone-treated HL-60 cells was similar to that in untreated cells.
These findings suggest that the inhibition of mitochondrial NADH dehydrogenase induces the differentiation of HL-60 cells but does not affect on the expression of the ND2 gene.The modulation of the cell surface antigen of HL-60 cells exposed to high dose of ND2 antisense DNA were indistinguishable from unexposed cells.
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