Journal
MICROVASCULAR RESEARCH
Volume 77, Issue 1, Pages 21-25Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mvr.2008.10.002
Keywords
Src tyrosine kinases; Caveolin-1; Dynamin-2; Caveolae; Pulmonary endothelium; Vascular permeability; Transcytosis
Categories
Funding
- NIH National Heart, Lung, and Blood Institute [HL71626, HL60678]
- American Heart Association [0730331N]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL071626, P01HL060678] Funding Source: NIH RePORTER
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Transcellular transport of albumin from the endothelial lumen to the abluminal perivascular interstitium via caveolae is a primary determinant of basal endothelial permeability. Albumin binding to specific caveolae-associated proteins induces the internalization of caveolae from the endothelial plasma membrane. Albumin-containing caveolae detach from the plasma membrane and traffic to the opposite membrane where they release albumin into the extravascular space. The events initiating transcytosis have been shown to be tightly regulated by Src family kinases, and thus Src signaling is thought to be a critical switch regulating caveolae-mediated transcellular transport of the plasma protein albumin. Recently, accumulating evidence indicates the importance of caveolae-mediated albumin transport in endothelial hyperpermeability in response to inflammatory stimuli. In this review, we focus on the current understanding of Src signaling in regulating basal permeability and inflammation-evoked increase in transcellular albumin permeability of the pulmonary endothelium. (C) 2008 Elsevier Inc. All rights reserved.
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