Molecular mechanisms of endothelial hyperpermeability: implications in inflammation.

Abstract:

:Endothelial hyperpermeability is a significant problem in vascular inflammation associated with trauma, ischaemia-reperfusion injury, sepsis, adult respiratory distress syndrome, diabetes, thrombosis and cancer. An important mechanism underlying this process is increased paracellular leakage of plasma fluid and protein. Inflammatory stimuli such as histamine, thrombin, vascular endothelial growth factor and activated neutrophils can cause dissociation of cell-cell junctions between endothelial cells as well as cytoskeleton contraction, leading to a widened intercellular space that facilitates transendothelial flux. Such structural changes initiate with agonist-receptor binding, followed by activation of intracellular signalling molecules including calcium, protein kinase C, tyrosine kinases, myosin light chain kinase, and small Rho-GTPases; these kinases and GTPases then phosphorylate or alter the conformation of different subcellular components that control cell-cell adhesion, resulting in paracellular hypermeability. Targeting key signalling molecules that mediate endothelial-junction-cytoskeleton dissociation demonstrates a therapeutic potential to improve vascular barrier function during inflammatory injury.

journal_name

Expert Rev Mol Med

authors

Kumar P,Shen Q,Pivetti CD,Lee ES,Wu MH,Yuan SY

doi

10.1017/S1462399409001112

subject

Has Abstract

pub_date

2009-06-30 00:00:00

pages

e19

issn

1462-3994

pii

S1462399409001112

journal_volume

11

pub_type

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