FIGURE 14. Vesicle endocytosis and transcytosis across endothelial cells.


Vesicle endocytosis and transcytosis across endothelial cells. Vesicle formation is triggered by Src kinase-mediated phosphorylation of caveolin-1 (cav-1) at the endothelial luminal membrane. Cav-1 subunits aggregate in lipid rafts and oligomerize to form caveolae. Other events, including albumin binding to the gp60 albumin receptor trigger vesicle endocytosis. Accessory proteins including dynamin and intersectin-2 are recruited to form the elongated neck of caveolae invaginations, which are then pinched off in response to Ras signaling to form enclosed vesicles. Vesicles remain docked to the inner surface of the cell membrane by vesicular (v)-SNARE binding to membrane-bound target (t)-SNARE, until docking is disrupted by the NEM-sensitive factor (NSF). Undocked vesicles may attach to microtubules via ATP-driven motor molecules (kinesin/dynein) that facilitate vesicle movement across the cell interior. Trafficking vesicles may fuse with VVOs, or may dock (via SNAREs) at the basolateral membrane and undergo membrane fusion and exocytosis, releasing contents into the extravascular space. This entire process is transcytosis.

From: Chapter 4, The Endothelial Barrier

Cover of Regulation of Endothelial Barrier Function
Regulation of Endothelial Barrier Function.
Yuan SY, Rigor RR.
San Rafael (CA): Morgan & Claypool Life Sciences; 2010.
Copyright © 2011 by Morgan & Claypool Life Sciences.

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