Görög P, Pearson J D
Atherosclerosis. 1984 Oct;53(1):21-9. doi: 10.1016/0021-9150(84)90101-1.
The surface sialic acid content of aortic endothelial cells in vitro was substantially lower in sparse cultures than at confluence. Binding of LDL to endothelial cells did not change at different culture densities and was unaffected by brief pretreatment with neuraminidase to partially remove surface sialic acid residues. In contrast, internalization of LDL declined by a factor of 3 between low density cell cultures and confluent monolayers; neuraminidase pretreatment increased LDL uptake and the effect was most marked (greater than 10-fold) at confluence. Pretreatment with cationised ferritin, which removed most of the surface sialic acid residues as well as glycosaminoglycans, increased LDL internalization by up to 20-fold, again with most effect on confluent monolayers. Thus LDL uptake is inversely correlated with sialic acid content. We conclude that changes in the surface density of sialic acid (and possibly other charged) residues significantly modulate endothelial LDL uptake, and suggest that focal increases in LDL accumulation during atherogenesis may be related to alterations in endothelial endocytic properties at sites of increased cell turnover or damage.
体外培养的主动脉内皮细胞表面唾液酸含量在稀疏培养时显著低于汇合状态。低密度脂蛋白（LDL）与内皮细胞的结合在不同培养密度下没有变化，并且用神经氨酸酶短暂预处理以部分去除表面唾液酸残基对其也没有影响。相反，低密度细胞培养物与汇合单层细胞之间，LDL的内化下降了3倍；神经氨酸酶预处理增加了LDL的摄取，且在汇合状态下效果最为显著（大于10倍）。用阳离子铁蛋白预处理，它去除了大部分表面唾液酸残基以及糖胺聚糖，使LDL内化增加了20倍，同样在汇合单层细胞上效果最为明显。因此，LDL摄取与唾液酸含量呈负相关。我们得出结论，唾液酸（可能还有其他带电荷的）残基表面密度的变化显著调节内皮细胞对LDL的摄取，并表明动脉粥样硬化形成过程中LDL积累的局部增加可能与细胞更新或损伤增加部位的内皮细胞内吞特性改变有关。
