| Project/Area Number |
60570555
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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 | Mie University |
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Principal Investigator |
KENKICHI Kita Faculty of Medicine, Mie University Assistant, 医学部, 助手 (90169847)
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| Co-Investigator(Kenkyū-buntansha) |
TORU Kita Faculty of Medicine, Kyoto University Assistant, 医学部, 助手 (60161460)
ISAO Tanaka Faculty of Medicine, Mie University Lecturer, 医学部附属病院, 講師 (20115710)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1986: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1985: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Cholesterol metabolism / LDL, Acetyl-LDL / LDL-receptor / Monocyte and macrophage / Monocytic differentiation / 単球分化 / 急性骨髄性白血病 |
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| Research Abstract |
In the present study, we established the methods for the detection of lipoprotein receptors and ACAT activity in rabbit and human macrophages as markers of cholesterol metabolism. Uptakes of various lipoproteins were different in species, for example <beta> -VLDL>acetyl-LDL>LDL in mouse, and <beta> -VLDL>LDL>acetyl-LDL in rabbit. This finding should be regarded to study chelesterol metabolism in terms of monocyte-macrophage differentiation. Relation between ACAT activity and Oil Red 0 staining in cultured cells with lipoproteins was sufficient. The study by Oil Red 0 staining could be performed smaller numbers of cells than by either receptor or ACTA assays. So, the results of this staing could be compared with those of other cytochemical and immunological studies even at the level of single cell.
In human monocytes, moderate or marked uptakes of either LDL or acetyl-LDL were observed by Oil Red 0 staining. Although other cytochemical and immunological markers did not change in cultured cells with TPA, stained granules increased in those cells with forming appearances. On the other hand, increase of acetyl-LDL showed in neither untreated nor cultured HL-60 cells, which are used for a model of monocytic differentiation in the in-vitro short term cultures with TPA, in spite of induction of nonspecific esterase and acidphosphatase activities. These results were also found in bona fide acute monocytic leukmia cells. This finding shows that HL-60 cells might not differentiate into macrophage completely.
Our results showed that the examination of cholesterol metabolism is feasible to provide the essential informations to either monocyte-macrophage differentiation or differentiational manners of leukemia cells.
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