Journal
TISSUE BARRIERS
Volume 3, Issue 1-2, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/21688370.2014.974448
Keywords
acute lung injury; barrier function; cytoskeleton; endothelial junctions; thrombin; pulmonary endothelium
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Funding
- Georgia Regents University [PO1HL0101902]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL101902] Funding Source: NIH RePORTER
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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.
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