Correlation of Lipoprotein Abnormalities in Childhood withe the Risk for Atherosclerotic Coronary Heart Disease (CAD) in Adulthood (Is abnormaltites in childhood a risk factor for CAD? )

儿童期脂蛋白异常与成年期动脉粥样硬化性冠心病 (CAD) 风险的相关性（儿童期异常是 CAD 的危险因素吗？）

• 批准号: 06670809
• 负责人: OHTA Takao
• 金额: $ 1.41万
• 依托单位: Kumamoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1994
• 资助国家: 日本
• 起止时间: 1994 至 1995
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670809/
• 关键词: LpA-I; A-II; Atherosclerosis; FERHDL; LDL size; Small LDL; small LDL; LDL size; LpA-1; A-II

1.We investigated the effects of subclasses of LpA-I [high density lipoprotein (HDL) containing only apoA-I] on cholesterol esterification in plasma and net cholestrol efflux from foam cells. LpA-I was composed of particles of three different sizes : large (Lg-LpA-I), medium (Md-LpA-I) and small (Sm-LpA-I). Plasma concentrations of LpA-I were positively correlated only with the level of Lg-LpA-I.Plasma concentrations of Lg-LpA-I were inversely correlated with the rate of cholesterol esterification in plasma and VLDL and LDL-depleted plasma (FERplasma and FER_<HDL>). When macrophage foam cells were incubated with Md-and Sm-LpA-I,cellular cholesterol mass was reduced by approximately 70%. In contrast, the cellular cholesterol-reducing capacity of Lg-LpA-I was negligible. Lg-LpA-I inhibited net cholesterol removal from foam cells that was mediated by Md-and Sm-LpA-I and cholesteryl ester production with these particles. These results suggest that Md-and Sm-LpA-I may actively participate i … More n cellular cholesterol removal and cholesterol esterification in plasma and HDL,while Lg-LpA-I may regulate these functions of Md-and Sm-LpA-I.2.We examined the correlations between low-density-lipoprotein (LDL) particle size and both FER_<HDL> and plasma lipid levels. FER_<HDL> and plasma triglyceride were negatively, and HDL-cholesterol was positively, correlated with LDL particle size (r=-0.728, -0.598and0.572, p>0.0001). Stepwise multiple regression analysis revealed that FER_<HDL> was most significantly associated with LDL particle size. Since FER_<HDL> is regulated by the plasma consentration of LpA-I (HDL containig apoA-I but not apoA-II), which is the anti-atherogenic fraction of HDL,the present results suggest that the regulation of LDL particle size may be part of the anti-atherogenic nature of LpA-1.3.Qualitative and quantitative changes of LpA-I in children with low plasma LpA-I were indistinguishable from those in patients with coronary artery disease (CAD) with low plasma LpA-I.All of our data suggest that children with low plasma LpA-I are high risk for CAD. Less

1.我们研究了LPA-I [仅含有ApoA-I]的LPA-I [高密度脂蛋白（HDL）的亚类对泡沫细胞中血浆和净胆固醇外排的胆固醇酯化的影响。 LPA-I由三种不同尺寸的颗粒组成：大（LG-LPA-I），培养基（MD-LPA-I）和小（SM-LPA-I）。 LPA-I的血浆浓度仅与LG-LPA-I水平正相关。 LG-LPA-I的血浆浓度与血浆和VLDL和LDL缺失的血浆（Ferplasma和Ferplasma和Fer_ <HDL>）中的胆固醇酯化率成反比。当将巨噬细胞泡沫细胞与MD和SM-LPA-I孵育时，细胞胆固醇质量的减少约70％。相反，LG-LPA-I的细胞胆固醇减少能力可以忽略不计。 LG-LPA-I抑制了从MD-LPA-I和胆固醇酯产生的泡沫细胞中去除的净胆固醇，并用这些颗粒产生。这些结果表明，MD和SM-LPA-I可能会积极参与I…血浆和HDL中更多的N细胞胆固醇去除和胆固醇酯化，而LG-LPA-I可能会调节MD-LPA-I.2的这些功能。2。我们检查了低密度 - 脂蛋白（LDL）粒子和lip lip and lip and lip and lip and lip and lip and lip and lip and lip and lip and y anm <hd。 FER_ <hdl>和血浆甘油三酸酯均为负面，HDL-胆固醇与LDL粒径相关（r = -0.728，-0.598和0.572，p> 0.0001）。逐步多元回归分析表明，FER_ <HDL>与LDL粒径最显着相关。由于FER_ <hdl>受LPA-I（HDL Containig apoA-I而非APOA-II）的血浆同意，这是HDL的抗动脉粥样硬化分数，因此本结果表明，LDL粒度的调节可能是LPA-1.的抗动脉基质性质的一部分。 LPA-I与血浆LPA-1低的冠状动脉疾病（CAD）患者没有区别。较少的

项目成果

Ikeda Yoichiro: "Interaction between apoA-I-containing lipoproteins and lecithin: cholesterol acyltransferase." Biochim Biophys Acta. 1215. 307-313 (1994)

池田洋一郎：“含 apoA-I 的脂蛋白与卵磷脂之间的相互作用：胆固醇酰基转移酶。”

Ohta Takao: "Structural and functional differences of subspecies of apoA-I-containing lipoproteins in patients with plasma cholesteryl ester transfer protein deficiency." J Lipid Res. 36. 696-704 (1995)

Ohta Takao：“血浆胆固醇酯转移蛋白缺乏症患者中含 apoA-I 的脂蛋白亚种的结构和功能差异。”

Kajikawa Mikio: "Lactoferrin inhibits cholesterol accumulation in macrophages mediated by acetylated or oxidized low density lipoproteins" Biochim Biophys Acta. 1213. 82-90 (1994)

Kajikawa Mikio：“乳铁蛋白抑制乙酰化或氧化低密度脂蛋白介导的巨噬细胞中胆固醇积累”Biochim Biophys Acta。

Takata Kouki: "A new case of apoA-I deficiency showing codon 8 nonsense mutation of the apoA-I gene without evidence of coronary heart disease" Arterioscler Thromb Vasc Biol. 15. 1866-1874 (1995)

Takata Kouki：“一例新的 apoA-I 缺乏症病例，显示 apoA-I 基因密码子 8 无义突变，但没有冠心病的证据”Arterioscler Thromb Vasc Biol。

Ikeda Yoichiro: "Interaction between apoA-I-containing lipoproteins and lecithin:cholesterol acyltransferase" Biochim Biophys Acta. 1215. 307-313 (1994)

池田阳一郎：“含 apoA-I 的脂蛋白与卵磷脂：胆固醇酰基转移酶之间的相互作用”Biochim Biophys Acta。