Schneeberger E E
Fed Proc. 1983 May 15;42(8):2419-24.
Plasma proteins interact with vascular endothelium in such a way as to render it less permeable to other macromolecules. Evidence from a variety of sources indicates that this may result from interaction of the circulating macromolecules with the negatively charged glycoprotein layer on the surface of endothelial cells, and that this layer may be responsible for some of the known molecular sieving properties attributed to the endothelium. Experiments with the fluorocarbon exchange-transfused rat are described, which suggest that there may be mechanisms other than vesicular translocation that facilitate the passage of macromolecules across endothelium. Such mechanisms include, among others, the formation of transient transendothelial channels that appear to be less sensitive than pinocytotic vesicles to the concentration of ambient protein. Recent evidence suggests that, in addition to molecular size and charge, glycosylation of protein molecules and cell membranes themselves may facilitate vesicular uptake.
血浆蛋白与血管内皮相互作用，使得血管内皮对其他大分子的通透性降低。来自各种来源的证据表明，这可能是由于循环中的大分子与内皮细胞表面带负电荷的糖蛋白层相互作用所致，并且该层可能是内皮细胞一些已知的分子筛分特性的原因。描述了用氟碳交换输血大鼠进行的实验，这些实验表明，除了囊泡转运外，可能还有其他机制促进大分子穿过内皮。这些机制包括，除其他外，形成短暂的跨内皮通道，这些通道似乎比胞饮小泡对周围蛋白质浓度的敏感性更低。最近的证据表明，除了分子大小和电荷外，蛋白质分子和细胞膜本身的糖基化可能促进囊泡摄取。
