| Project/Area Number |
62480134
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Medical College of Oita |
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Principal Investigator |
KUWANO Michihiko Medical College of Oita, Professor, 医学部, 教授 (80037431)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Tatsuo Medical College of Oita, Assistant Professor, 医学部, 助教授 (80080555)
ONO Mayumi Medical College of Oita, Assistant, 医学部, 助手 (80128347)
島田 達生 大分医科大学, 医学部・解剖学, 助教授 (60136786)
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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 |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1988: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1987: ¥5,600,000 (Direct Cost: ¥5,600,000)
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| Keywords | Low density lipoprotein / LDL receptor / LDL receptor mutation / Cholesterol metabolic disorders / Carbohydrate chain mutation / Macrophage / 泡沫化細胞 / 低比重リポ蛋白(LDL) / 糖鎖構造異変 / 体細胞遺伝変異 / 低比重リポ蛋白レセプター不全 / ゴルジ装置 |
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| Research Abstract |
Hypercholesterolemia and atherosclerosis are plausibly main origins for hypertension. We have established two systems of model cell lines in culture for altered cholesterol metabolic disease and also atheromatous foam cells.
First system is to establish and characterize somatic cell mutants with defects in the regulation of sterol metabolism. We have selected animal cell mutants with very high sterol synthesis, and they carry low density lipoprotein (LDL) receptors with altered sugar chains. These mutants are supposed to affect Golgi apparatus function. discovery of this new gene, int, may imply a further etiology for hypercholesterolemia.
Second system is to study mechanism for appearance of atheromatous foam cells by using established mouse macrophage J774 cell line in culture. J774 cells are loaded with cholesterol esters when native LDL is challenged. Analysis of biosynthesis, processing and degradation of LDL receptors of J774 cells shows very rapid rate of degradation of LDL receptors in comparison with other non-macrophage cell lines. This model system with macrophage cell line might imply new idea for involvement of native LDL in earlier atherosclerosis change besides scavenger pathway model with denatured LDL.
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