ABNORMAL CELL INTERACTIVE PROPERTIES OF LOW-DENSITY LIPOPROTEINS ISOLATED FROM PATIENTS WITH CHRONIC RENAL-FAILURE
ABNORMAL CELL INTERACTIVE PROPERTIES OF LOW-DENSITY LIPOPROTEINS ISOLATED FROM PATIENTS WITH CHRONIC RENAL-FAILURE
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DOI：
10.1016/0026-0495(85)90052-6
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发表时间：
1985-01-01
影响因子：
9.8
通讯作者：
SCHONFELD, G
中科院分区：
文献类型：
--
作者：
GONEN, B;GOLDBERG, AP;SCHONFELD, G
维持性血液透析的肾功能衰竭患者动脉粥样硬化的发生率加快。这一点，以及化学修饰的低密度脂蛋白（LDL）比天然LDL具有更好的刺激血管壁巨噬细胞内胆固醇酯积累的能力，导致慢性尿毒症患者可能发生apo-LDL的某些改变。从18名慢性肾功能衰竭患者和13名血脂正常的对照者中分离LDL（[密度] = 1.019-1.063 g/ml），并比较不同LDL制剂与培养的成纤维细胞的相互作用特性。与正常LDL相比，尿毒症LDL结合较少，降解较少，刺激成纤维细胞中胆固醇酯形成的能力减弱。LDL氨甲酰化在体外表现出与成纤维细胞类似的尿毒症LDL的相互作用特性。与正常LDL相似，尿毒症LDL不被大鼠腹腔巨噬细胞上的清道夫受体吸收。然而，尿毒症LDL的成纤维细胞摄取的减少可能会增加这些颗粒在血管壁内皮下区域内的停留时间，最终导致动脉粥样硬化性增加。体内apoB赖氨酸残基的氨甲酰化、由于缺乏功能性肾组织而导致的LDL的异常catalysis或LDL的甘油三酯富集是尿毒症LDL的异常性质的可能解释。
Patients with renal failure on maintenance hemodialysis have accelerated rate of atherosclerosis. This, and the fact that chemically modified low density lipoproteins (LDL) have a better capacity than native LDL to stimulate cholesteryl ester accumulation within macrophages in the vessel wall, led to the possibility that some alteration in apo-LDL may take place in chronically uremic patients. LDL ([density] = 1.019-1.063 g/ml) was isolated from 18 patients with chronic renal failure and from 13 normolipidemic controls and compared the interactive properties of the different LDL preparations with cultured fibroblasts. Uremic LDL associates less, is degraded less and has diminished ability to stimulate cholesteryl ester formation in fibroblasts when compared to normal LDL. LDL carbamylated in vitro showed interactive properties with fibroblasts similar to those of uremic LDL. Uremic LDL was not taken up by scavenger receptors present on rat peritoneal macrophages, similarly to normal LDL. However, the decrease in uptake by fibroblasts of uremic LDL may increase the residence time of these particles within the subendothelial region of the vessel wall, ultimately resulting in increased atherogenicity. Carbamylation of lysine residues of apoB in vivo, abnormal catabolism of LDL due to the absence of functional renal tissue, or triglyceride enrichment of LDL are among the possible explanations for the abnormal properties of uremic LDL.