Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury

Anita Kása; Csilla Csortos; Alexander D. Verin

doi:10.4161/21688370.2014.974448

Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury

Anita Kása, Csilla Csortos, Alexander D. Verin

Research output: Contribution to journal › Review article › peer-review

79 Scopus citations

Abstract

Endothelial cells (EC) form a semi-permeable barrierbetween the interior space of blood vessels and theunderlying tissues. In acute lung injury (ALI) the EC barrier isweakened leading to increased vascular permeability. It iswidely accepted that EC barrier integrity is criticallydependent upon intact cytoskeletal structure and celljunctions. Edemagenic agonists, like thrombin or endotoxinlipopolysaccharide (LPS), induced cytoskeletal rearrangement,and EC contractile responses leading to disruption ofintercellular contacts and EC permeability increase. The highlyclinically-relevant cytoskeletal mechanisms of EC barrierdysfunction are currently under intense investigation and willbe described and discussed in the current review.

Original language	English (US)
Journal	Tissue Barriers
Volume	3
Issue number	1
DOIs	https://doi.org/10.4161/21688370.2014.974448
State	Published - 2015

Keywords

Acute lung injury
Barrier function
Cytoskeleton
Endothelial junctions
Pulmonary endothelium
Thrombin

ASJC Scopus subject areas

Biochemistry
Histology
Cell Biology

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10.4161/21688370.2014.974448

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title = "Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury",

abstract = "Endothelial cells (EC) form a semi-permeable barrierbetween the interior space of blood vessels and theunderlying tissues. In acute lung injury (ALI) the EC barrier isweakened leading to increased vascular permeability. It iswidely accepted that EC barrier integrity is criticallydependent upon intact cytoskeletal structure and celljunctions. Edemagenic agonists, like thrombin or endotoxinlipopolysaccharide (LPS), induced cytoskeletal rearrangement,and EC contractile responses leading to disruption ofintercellular contacts and EC permeability increase. The highlyclinically-relevant cytoskeletal mechanisms of EC barrierdysfunction are currently under intense investigation and willbe described and discussed in the current review.",

keywords = "Acute lung injury, Barrier function, Cytoskeleton, Endothelial junctions, Pulmonary endothelium, Thrombin",

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AU - Kása, Anita

AU - Csortos, Csilla

AU - Verin, Alexander D.

N1 - Funding Information: This manuscript was supported by grant PO1HL0101902 from the National Institute of Health and Extramural Success Award from the Georgia Regents University. Publisher Copyright: © 2015 Taylor & Francis Group, LLC.

PY - 2015

Y1 - 2015

N2 - Endothelial cells (EC) form a semi-permeable barrierbetween the interior space of blood vessels and theunderlying tissues. In acute lung injury (ALI) the EC barrier isweakened leading to increased vascular permeability. It iswidely accepted that EC barrier integrity is criticallydependent upon intact cytoskeletal structure and celljunctions. Edemagenic agonists, like thrombin or endotoxinlipopolysaccharide (LPS), induced cytoskeletal rearrangement,and EC contractile responses leading to disruption ofintercellular contacts and EC permeability increase. The highlyclinically-relevant cytoskeletal mechanisms of EC barrierdysfunction are currently under intense investigation and willbe described and discussed in the current review.

AB - Endothelial cells (EC) form a semi-permeable barrierbetween the interior space of blood vessels and theunderlying tissues. In acute lung injury (ALI) the EC barrier isweakened leading to increased vascular permeability. It iswidely accepted that EC barrier integrity is criticallydependent upon intact cytoskeletal structure and celljunctions. Edemagenic agonists, like thrombin or endotoxinlipopolysaccharide (LPS), induced cytoskeletal rearrangement,and EC contractile responses leading to disruption ofintercellular contacts and EC permeability increase. The highlyclinically-relevant cytoskeletal mechanisms of EC barrierdysfunction are currently under intense investigation and willbe described and discussed in the current review.

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KW - Barrier function

KW - Cytoskeleton

KW - Endothelial junctions

KW - Pulmonary endothelium

KW - Thrombin

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Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury

Abstract

Keywords

ASJC Scopus subject areas

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