Sviridov D D, Safonova I G, Tsybulsky V P, Talalaev A G, Preobrazensky S N, Repin V S, Smirnov V N
Biochim Biophys Acta. 1987 Jun 23;919(3):266-74. doi: 10.1016/0005-2760(87)90266-9.
The effect of cholesterol on the interaction of high-density lipoprotein (HDL) with isolated human small intestine epithelial cells (enterocytes) was studied. 125I-labeled HDL3 binding by these cells was enhanced in response to cholesterol loading of the cells in a time- and dose- dependent manner. Preincubation of the cells with cholesterol led to the enhancement both of the number of binding sites and the binding affinity. The enhancement of binding correlated with the cellular cholesterol content. Cycloheximide (0.5 mM) inhibited uptake of cholesterol by enterocytes and blocked its effect on 125I-labeled HDL3 binding. The effect of cholesterol on 125I-labeled HDL3 degradation had a double-phase character. At concentrations 10-20 micrograms/ml, the degradation rate was rapidly elevated, but further increase in cholesterol concentration led to a fall in the degradation rate. Incubation of enterocytes with HDL3 resulted in the efflux of cholesterol from cells and its incorporation into HDL3. The results obtained make it possible to assume that binding and degradation of 125I-labeled HDL3 by human enterocytes are independently regulated by the cell total cholesterol content. Binding of HDL by enterocytes may result both in the degradation of HDL and cholesterol efflux from cells.
研究了胆固醇对高密度脂蛋白（HDL）与分离的人小肠上皮细胞（肠细胞）相互作用的影响。这些细胞对125I标记的HDL3的结合随着细胞胆固醇负荷的增加呈时间和剂量依赖性增强。用胆固醇对细胞进行预孵育导致结合位点数量和结合亲和力均增强。结合的增强与细胞胆固醇含量相关。环己酰亚胺（0.5 mM）抑制肠细胞对胆固醇的摄取并阻断其对125I标记的HDL3结合的影响。胆固醇对125I标记的HDL3降解的影响具有双相特征。在浓度为10 - 20微克/毫升时，降解速率迅速升高，但胆固醇浓度进一步增加导致降解速率下降。用HDL3孵育肠细胞导致胆固醇从细胞中流出并掺入HDL3中。所得结果使得可以假设人肠细胞对125I标记的HDL3的结合和降解由细胞总胆固醇含量独立调节。肠细胞对HDL的结合可能导致HDL的降解以及胆固醇从细胞中流出。
