| Literature DB >> 25838980 |
Anita Kása1, Csilla Csortos2, Alexander D Verin3.
Abstract
Endothelial cells (EC) form a semi-permeable barrier between the interior space of blood vessels and the underlying tissues. In acute lung injury (ALI) the EC barrier is weakened leading to increased vascular permeability. It is widely accepted that EC barrier integrity is critically dependent upon intact cytoskeletal structure and cell junctions. Edemagenic agonists, like thrombin or endotoxin lipopolysaccharide (LPS), induced cytoskeletal rearrangement, and EC contractile responses leading to disruption of intercellular contacts and EC permeability increase. The highly clinically-relevant cytoskeletal mechanisms of EC barrier dysfunction are currently under intense investigation and will be described and discussed in the current review.Entities:
Keywords: AJ, adherens junction; ALI, Acute Lung Injury; ARDS, Acute Respiratory Distress Syndrome; CPI-17, PKC potentiated inhibitory protein of 17 kDa; CaD, caldesmon; EC, endothelial cells; GJ, gap junction; HSP-27, small heat shock actin-capping protein of 27 kDa; IL, interleukin; LPS, lipopolysaccharide; MLC, myosin light chain; MLCK, Ca2+/calmodulin (CaM) dependent MLC kinase; MLCP, myosin light chain phosphatase; MT, microtubules; MYPT1, myosin phosphatase targeting subunit 1; PKA, protein kinase A; PKC, protein kinase C; SM, smooth muscle; TJ, tight junction; TLR4, toll-like receptor 4; TNFα, tumor necrosis factor α; acute lung injury; barrier function; cytoskeleton; endothelial junctions; pulmonary endothelium; thrombin
Year: 2015 PMID： 25838980 PMCID： PMC4372017 DOI： 10.4161/21688370.2014.974448
Source DB: PubMed Journal: Tissue Barriers ISSN： 2168-8362