并行传输
跨细胞
小窝
跨细胞
细胞生物学
内皮干细胞
血管通透性
小窝蛋白1
内皮
化学
生物
磁导率
细胞
生物化学
信号转导
内分泌学
内吞作用
膜
体外
作者
Yu Sun,Richard D. Minshall,Guochang Hu
出处
期刊:Methods in molecular biology
日期:2011-01-01
卷期号:: 303-317
被引量:20
标识
DOI:10.1007/978-1-61779-191-8_21
摘要
Endothelial permeability measurements of intact vascular beds and monolayer cultures are used to describe transport of small molecules (ions, water, and nutrients), macromolecules and plasma protein across the vascular endothelia. Disruption of the endothelial barrier leads to vascular hyperpermeability and protein-rich edema which is a key hallmark of inflammation. Transport of the most abundant plasma protein, albumin, occurs by means of transcellular and paracellular pathways. In healthy, noninflamed vessels, endothelial cell–cell contacts significantly restrict the paracellular permeability of albumin, whereas its transcellular transport from the blood to the abluminal perivascular interstitium occurs via caveolae. Thus, caveolae-mediated transport is a primary determinant of the basal endothelial permeability properties. Increased paracellular permeability induced during inflammation is thought to be due to the opening of interendothelial cell–cell junctions and disruption of endothelial cell–matrix contacts within the vasculature. We recently demonstrated that caveolae-mediated transendothelial transport (transcytosis) of macromolecules through the microvascular endothelial barrier is also an important mechanism responsible for inflammation-evoked pulmonary vascular hyperpermeability and protein-rich edema formation. Moreover, caveolin-1, a structural and scaffolding protein required for caveolae formation and transcellular transport, also plays an important role in oxidant-induced paracellular hyperpermeability. This review highlights the methods used to assess transcellular and paracellular permeability properties of the intact mouse lung and cultured endothelial cell monolayers.
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