作者: D P Baker , B J Van Lenten , A M Fogelman , P A Edwards , C Kean
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摘要: Primary and first passage aortic endothelial cells were shown to possess a high affinity receptor for beta-migrating very low density lipoproteins (beta-VLDL) distinct from the lipoprotein (LDL) scavenger on these cells. In bovine cells, 125I-rabbit beta-VLDL was taken up degraded by process that competed unlabeled rabbit postprandial VLDL fat-fed normal subject. However, human or LDL, LDL modified malondialdehyde (MDA-LDL), fasted not effective competitors degradation of beta-VLDL. contrast receptor-mediated 125I-human 125I-human-MDA-LDL, cell did affect Endothelial Watanabe heritable hyperlipidemic (WHHL) virtually degrade but at rate equal seen in It concluded is genetically receptor. Incubation 3 days with 100 micrograms/ml protein caused an 88% increase cellular cholesterol content, even though activity down-regulated 60%. monocyte-macrophages are thus far only known receptor,