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The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Regulation of Endothelial Junctional Permeability

Vandenbroucke, Emily, Mehta, Dolly, Minshall, Richard, Malik, Asrar B.·2008·Annals of the New York Academy of Sciences

Abstract

The endothelium is a semi‐permeable barrier that regulates the flux of liquid and solutes, including plasma proteins, between the blood and surrounding tissue. The permeability of the vascular barrier can be modified in response to specific stimuli acting on endothelial cells. Transport across the endothelium can occur via two different pathways: through the endothelial cell (transcellular) or between adjacent cells, through interendothelial junctions (paracellular). This review focuses on the regulation of the paracellular pathway. The paracellular pathway is composed of adhesive junctions between endothelial cells, both tight junctions and adherens junctions. The actin cytoskeleton is bound to each junction and controls the integrity of each through actin remodeling. These interendothelial junctions can be disassembled or assembled to either increase or decrease paracellular permeability. Mediators, such as thrombin, TNF‐α, and LPS, stimulate their respective receptor on endothelial cells to initiate signaling that increases cytosolic Ca 2+ and activates myosin light chain kinase (MLCK), as well as monomeric GTPases RhoA, Rac1, and Cdc42. Ca 2+ activation of MLCK and RhoA disrupts junctions, whereas Rac1 and Cdc42 promote junctional assembly. Increased endothelial permeability can be reversed with “barrier stabilizing agents,” such as sphingosine‐1‐phosphate and cyclic adenosine monophosphate (cAMP). This review provides an overview of the mechanisms that regulate paracellular permeability.

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Crossref · 10.1196/annals.1420.016

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Metadata

Authors
Vandenbroucke, E., Mehta, D., Minshall, R., & Malik, A. B.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2008-03
Volume
1123
Issue
1
Pages
134-145
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1969448383
Cited by
596
References
3
FWCI
25.66
Type
journal article
Language
en
Open access
closed

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