首页> 美国卫生研究院文献>The Journal of Clinical Investigation >The Interaction of Serum and Arterial Lipoproteins with Elastin of the Arterial Intima and Its Role in the Lipid Accumulation in Atherosclerotic Plaques
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The Interaction of Serum and Arterial Lipoproteins with Elastin of the Arterial Intima and Its Role in the Lipid Accumulation in Atherosclerotic Plaques

机译:血清和动脉脂蛋白与动脉内膜弹性蛋白的相互作用及其在动脉粥样硬化斑块中脂质蓄积中的作用

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摘要

Arterial elastin appears to be a proteinlipid complex with the lipid component being bound to elastin peptide groups. In atherosclerotic lesions the lipid content of elastin increases progressively with increasing severity of atherosclerosis. The increases in the lipid content of plaque elastin are mainly due to large increases in cholesterol with about 80% of the cholesterol being cholesterol ester. This deposition of cholesterol in elastin accounts for a substantial part of the total cholesterol accumulation in atherosclerotic lesions of all stages. The present in vitro study suggests that the mechanism involved in the deposition of lipids in arterial elastin may be an interaction of the elastin protein with serum or arterial low density or very low density lipoproteins (LDL and VLDL) resulting in a transfer of lipids, but not of lipoprotein protein to the elastin. No significant lipid transfer occurred from the high density lipoproteins or chylomicrons. The amount of lipid taken up by plaque elastin was strikingly higher than by normal elastin and consisted mainly of cholesterol with over 80% of the cholesterol being cholesterol ester. The precondition for the lipid accumulation in plaque elastin appeared to be an altered amino acid composition of the elastin protein consisting of an increase in polar amino acids and a reduction in cross-linking amino acids. Subsequent treatment of lipoprotein-incubated arterial elastin with hot alkali and apolipoproteins did not reverse the binding of lipoprotein lipid to diseased elastin.
机译:动脉弹性蛋白似乎是一种蛋白脂质复合物,脂质成分与弹性蛋白肽基团结合。在动脉粥样硬化病变中,弹性蛋白的脂质含量随着动脉粥样硬化严重程度的增加而逐渐增加。斑块弹性蛋白的脂质含量的增加主要是由于胆固醇的大量增加,其中约80%的胆固醇为胆固醇酯。胆固醇在弹性蛋白中的这种沉积占所有阶段的动脉粥样硬化病变中总胆固醇积累的很大一部分。目前的体外研究表明,脂质在动脉弹性蛋白中沉积的机制可能是弹性蛋白与血清或动脉低密度或极低密度脂蛋白(LDL和VLDL)的相互作用,导致脂质转移,但脂蛋白不是弹性蛋白。高密度脂蛋白或乳糜微粒未发生明显的脂质转移。斑块弹力蛋白吸收的脂质量显着高于正常弹力蛋白,并且主要由胆固醇组成,其中超过80%的胆固醇为胆固醇酯。斑块弹性蛋白中脂质积累的前提条件似乎是弹性蛋白蛋白质的氨基酸组成发生了变化,包括极性氨基酸的增加和交联氨基酸的减少。用热碱和载脂蛋白对脂蛋白孵育的动脉弹性蛋白进行后续处理,不会逆转脂蛋白脂质与患病弹性蛋白的结合。

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