- Author:
	        		
		        		
		        		
			        		Jong J AHN
			        		
			        		
			        		
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			        		Jong P JUNG
			        		
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			        		Soon E PARK
			        		
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			        		Minhyun LEE
			        		
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			        		Byungsuk KWON
			        		
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			        		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.
 
            
