Vlodavsky I, Fielding P E, Fielding C J, Gospodarowicz D
Proc Natl Acad Sci U S A. 1978 Jan;75(1):356-60. doi: 10.1073/pnas.75.1.356.
Bovine vascular endothelial cells during logarithmic growth bind, internalize, and degrade low density lipoprotein (LDL) via a receptor-mediated pathway. However, contact-inhibited (confluent) monolayers bind but do not internalize LDL. This is in contrast to aortic smooth muscle cells or endothelial cells that have lost the property of contact inhibition. These cells internalize and degrade LDL at both high and low cell densities. The LDL receptors of smooth muscle and sparse endothelial cells down-regulate in response to LDL. In contrast, normal endothelial cells at confluency show little response. When contact inhibition in endothelial monolayers was locally released by wounding, and LDL was present, only cells released from contact inhibition accumulated LDL cholesterol. In smooth muscle cells under the same conditions, the entire culture interiorized lipid. It thus appears that in endothelial cells, unlike smooth muscle cells, contact inhibition is the major factor regulating cellular uptake of LDL cholesteryl ester. Reversal of contact inhibition by wounding provides a mechanism by which the endothelium could be the primary initiator of the atherosclerotic plaque.
对数生长期的牛血管内皮细胞通过受体介导的途径结合、内化并降解低密度脂蛋白（LDL）。然而，接触抑制（汇合）的单层细胞能结合LDL，但不会将其内化。这与失去接触抑制特性的主动脉平滑肌细胞或内皮细胞形成对比。这些细胞在高细胞密度和低细胞密度下都会内化并降解LDL。平滑肌细胞和稀疏内皮细胞的LDL受体在LDL作用下会下调。相比之下，汇合状态下的正常内皮细胞几乎没有反应。当通过创伤局部解除内皮单层细胞的接触抑制且存在LDL时，只有从接触抑制中释放出来的细胞会积累LDL胆固醇。在相同条件下的平滑肌细胞中，整个培养物都会内化脂质。因此，与平滑肌细胞不同，在内皮细胞中，接触抑制似乎是调节细胞摄取LDL胆固醇酯的主要因素。创伤导致的接触抑制逆转提供了一种机制，通过该机制内皮可能成为动脉粥样硬化斑块的主要起始部位。
