- Author:
Jong J AHN
1
;
Jong P JUNG
;
Soon E PARK
;
Minhyun LEE
;
Byungsuk KWON
;
Hong R CHO
Author Information
- Publication Type:In Vitro ; Brief Communication
- Keywords: Acute lung injury; Protein kinase C-delta; Vascular permeability
- MeSH: Acute Lung Injury*; Animals; Capillary Permeability*; Endothelial Cells; Lung; Mice; Mortality; Neutrophils; Protein Kinase C-delta*; Protein Kinases*; Pulmonary Edema
- From:Immune Network 2015;15(4):206-211
- CountryRepublic of Korea
- Language:English
- Abstract: Pulmonary edema is a major cause of mortality due to acute lung injury (ALI). The involvement of protein kinase C-delta (PKC-delta) in ALI has been a controversial topic. Here we investigated PKC-delta function in ALI using PKC-delta knockout (KO) mice and PKC inhibitors. Our results indicated that although the ability to produce proinflammatory mediators in response to LPS injury in PKC-delta KO mice was similar to that of control mice, they showed enhanced recruitment of neutrophils to the lung and more severe pulmonary edema. PKC-delta inhibition promoted barrier dysfunction in an endothelial cell layer in vitro, and administration of a PKC-delta-specific inhibitor significantly increased steady state vascular permeability. A neutrophil transmigration assay indicated that the PKC-delta inhibition increased neutrophil transmigration through an endothelial monolayer. This suggests that PKC-delta inhibition induces structural changes in endothelial cells, allowing extravasation of proteins and neutrophils.