Involvement of Protein Kinase C-δ in Vascular Permeability in Acute Lung Injury

Immune Network
Jong J AhnHong R Cho

Abstract

Pulmonary edema is a major cause of mortality due to acute lung injury (ALI). The involvement of protein kinase C-δ (PKC-δ) in ALI has been a controversial topic. Here we investigated PKC-δ function in ALI using PKC-δ knockout (KO) mice and PKC inhibitors. Our results indicated that although the ability to produce proinflammatory mediators in response to LPS injury in PKC-δ KO mice was similar to that of control mice, they showed enhanced recruitment of neutrophils to the lung and more severe pulmonary edema. PKC-δ inhibition promoted barrier dysfunction in an endothelial cell layer in vitro, and administration of a PKC-δ-specific inhibitor significantly increased steady state vascular permeability. A neutrophil transmigration assay indicated that the PKC-δ inhibition increased neutrophil transmigration through an endothelial monolayer. This suggests that PKC-δ inhibition induces structural changes in endothelial cells, allowing extravasation of proteins and neutrophils.

References

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Citations

Nov 3, 2016·American Journal of Physiology. Lung Cellular and Molecular Physiology·Nektarios BarabutisJohn D Catravas
Oct 10, 2020·BMC Pulmonary Medicine·Maurizio TurzoCornelius J Busch

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Methods Mentioned

BETA
Protein Assay
Assay

Software Mentioned

GraphPad Prism

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