Abstract
Many macromolecules are unable to enter cells by passage across the plasma membrane and instead are captured and internalised by endocytosis. The presence of abundant endocytic, or pinocytic, vesicles in the cytoplasm of endothelial cells was first reported in electron micrographs by Palade (31). Their existence suggested involvement in the transendothelial passage of macromolecules across the endothelial barrier in vesicles (32), the contents of which subsequently appear in the subendothelial space. This process occurs as an alternative to passage of macromolecules via endothelial cell junctions (38). Thus, the vesicular and junctional pathways became the structural equivalents of, respectively, the large and small pore systems of vascular transport as postulated from physiological tracer studies (4, 33, 38, 39). The contribution of vesicular transport to transendothelial macromolecular flux is still unclear, despite considerable efforts in characterising this system. Transendothelial transport has been primarily investigated in the microcirculation with very few studies of large artery endothelium. While the study of transendothelial transport in vitro presents a number of technical problems, measurement of endocytosis rates and their regulation provides insights into cellular events which are directly relevant to vesicular transport. In addition to its postulated transport function, endocytosis is also related to the metabolic needs (and functional integrity) of the endothelial cell. As is clear from much of the work reported elsewhere in this volume, the endothelium plays a key role in the maintenance of vessel wall homeostasis and interest in arterial endothelial endocytosis in particular is related to its involvement in the pathogenesis of atherosclerosis. Endocytosis in endothelial cells is therefore of importance from the standpoint of both normal and pathological events.
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Davies, P.F. (1984). Quantitative aspects of endocytosis in cultured endothelial cells. In: Jaffe, E.A. (eds) Biology of Endothelial Cells. Developments in Cardiovascular Medicine, vol 27. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2825-4_37
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