Inflammatory Cytokines in Vascular Dysfunction and Vascular Disease

Molecular basis of the inner blood-retinal barrier and its breakdown in diabetic macular edema and other pathological conditions.

Increased lung vascular permeability is an important contributor to respiratory failure in acute lung injury (ALI). We found that a function-blocking antibody against the integrin αvβ5 prevented development of lung vascular permeability in two different models of ALI: ischemia-reperfusion in rats (mediated by vascular endothelial growth factor [VEGF]) and ventilation-induced lung injury (VILI) in mice (mediated, at least in part, by transforming growth factor-β [TGF-β]). Knockout mice homozygous for a null mutation of the integrin β5 subunit were also protected from lung vascular permeability in VILI. In pulmonary endothelial cells, both the genetic absence and blocking of αvβ5 prevented increases in monolayer permeability induced by VEGF, TGF-β, and thrombin. Furthermore, actin stress fiber formation induced by each of these agonists was attenuated by blocking αvβ5, suggesting that αvβ5 regulates induced pulmonary endothelial permeability by facilitating interactions with the actin cytoskeleton. These results identify integrin αvβ5 as a central regulator of increased pulmonary vascular permeability and a potentially attractive therapeutic target in ALI.

/pdf/integrin-avb5-regulates-lung-vascular-permeability-and-4ajoevug5i.pdf

Integrin αvβ5 Regulates Lung Vascular Permeability and Pulmonary Endothelial Barrier Function

Acute lung injury: The therapeutic role of Rho kinase inhibitors.

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.

https://www.tandfonline.com/doi/pdf/10.4161/21688370.2014.974448

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

Lung edema due to increased vascular permeability is a hallmark of acute lung injury and acute respiratory distress syndrome. Both p38 and RhoA signaling events are involved in transforming growth ...

Transforming growth factor-β1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation

activation and subsequent RhoA activation barrier dysfunction involves Smad2-dependent p38

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Transforming growth factor-β1-induced endothelial barrier dysfunction involves Smad2-dependent p38 activation and subsequent RhoA activation

activation and subsequent RhoA activation barrier dysfunction involves Smad2-dependent p38