The interaction of the high-density lipoprotein with cultured cells of bovine vascular endothelium.
The interaction of the high-density lipoprotein with cultured cells of bovine vascular endothelium.
复制标题
高密度脂蛋白与培养的牛血管内皮细胞的相互作用。
DOI：
10.1111/j.1432-1033.1981.tb05611.x
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Gospodarowicz,D
中科院分区：
文献类型：
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作者：
Tauber,JP;Goldminz,D;Vlodavsky,I;Gospodarowicz,D
先前的研究表明，高密度脂蛋白（HDL）对低密度血管内皮细胞培养物具有促有丝分裂作用。相反，生理浓度的低密度脂蛋白（LDL）对该细胞类型具有细胞毒性[Tauber et al.（1980）J.Clin.Invest. 66，696 - 709]。为了将这些观察结果与这些脂蛋白与细胞相互作用后发生的物理化学事件联系起来，我们研究了HDL的结合、内化和降解作为细胞密度和组织的函数，并将结果与LDL的结果进行了比较。培养的血管内皮细胞结合HDL的程度，以摩尔为基础，与LDL相似。由于预先暴露于LDL的细胞中LDL受体位点的80%损失与HDL结合的可检测减少无关，因此HDL和LDL结合位点可能作为不同的实体存在于细胞表面上。在减少125 I-HDL的结合方面，LDL超过125 I-HDL 5 - 10倍摩尔过量几乎与类似过量的未标记HDL一样有效，表明LDL可以与HDL结合。相比之下，在存在50倍摩尔过量的未标记HDL的情况下，125I-LDL结合和摄取减少不到20%。高密度脂蛋白的吸收和降解均比低密度脂蛋白低10 - 20倍。在几乎完全抑制LDL降解的浓度下，氯喹仅轻微或不抑制HDL降解。融合和高度有机化的内皮细胞培养物结合HDL和LDL颗粒的程度是稀疏或亚融合培养物结合量的一半。静息内皮细胞单层的形成仅与HDL摄取降低2倍相关，而LDL摄取和降解降低10 - 20倍。在稀疏和汇合的内皮细胞培养物中，通过流体胞饮非特异性吸附性内吞作用的摄取可以解释大部分HDL摄取。当以高浓度添加到稀疏和活跃生长的培养物中时，HDL内化的不同途径。
Previous studies have shown that high‐density lipoprotein (HDL) is mitogenic for low‐density vascular endo thelial cell cultures. In contrast, low‐density lipoprotein(LDL) at physiological concentration is cytotoxic for this cell type [Tauber et al. (1980)J.Clin.Invest. 66, 696‐709]. In order to relate these observations to the physico‐chemical events occurring after the interaction of these lipoproteins with the cells, we have studied the binding, internalization, and degradation of HDL as a function of cell density and organization and have compared the results to those obtained with LDL.Cultured vascular endothelial cells bind HDL to an extent which, on a molar basis, is similar to that of LDL. Since an 80% loss of the LDL receptor sites in cells that were preexposed to LDL was not associated with a detectable decrease in HDL binding, it is likely that HDL and LDL binding sites exist on the cell surface as distinct entities A 5‐10 fold molar excess of LDL over125I‐HDL was almost as effective as a similar excess of unlabeled HDL in reducing the binding of125, indicationg that LDL can comete with HDL for HDL binding sites. In contrast,125I‐LDL binding and uptake were reduced by less than 20% in the presence of a 50‐fold molar excess of unlabeled HDL. Both uptake and degradation of HDL were 10‐20 fold lower than those of LDL. HDL degradation was only slightly or not inhibited by chloroquine at a concentration which almost fully inhibited the degradation of LDL. Confluent and highly orgainized endothelial cell cultures bind HDL and LDL particles to an extent which is half of the amount bound to sparse or subconfluent culture However. The formation of a resting endothelial cell monlayer was associated with only a twofold decrease in the uptake of HDL, as compard to a 10‐20‐fold decrease in the uptake and degradation of LDL. In both sparse and confluent endothelial cultures, uptake via fluid pinocytosis non‐specific adscorptive endocytosis could account for most of the HDL uptake. The different pathways of internalization of HDL when added at high concentration to sparse and actively growing cultures.