http://purl.uniprot.org/citations/22983354 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/22983354 | http://www.w3.org/2000/01/rdf-schema#comment | "The pathogenesis of acute lung injury and acute respiratory distress syndrome is characterized by sequestration of leukocytes in lung tissue, disruption of capillary integrity, and pulmonary edema. PKCδ plays a critical role in RhoA-mediated endothelial barrier function and inflammatory responses. We used mice with genetic deletion of PKCδ (PKCδ(-/-)) to assess the role of PKCδ in susceptibility to LPS-induced lung injury and pulmonary edema. Under baseline conditions or in settings of increased capillary hydrostatic pressures, no differences were noted in the filtration coefficients (k(f)) or wet-to-dry weight ratios between PKCδ(+/+) and PKCδ(-/-) mice. However, at 24 h after exposure to LPS, the k(f) values were significantly higher in lungs isolated from PKCδ(+/+) than PKCδ(-/-) mice. In addition, bronchoalveolar lavage fluid obtained from LPS-exposed PKCδ(+/+) mice displayed increased protein and cell content compared with LPS-exposed PKCδ(-/-) mice, but similar changes in inflammatory cytokines were measured. Histology indicated elevated LPS-induced cellularity and inflammation within PKCδ(+/+) mouse lung parenchyma relative to PKCδ(-/-) mouse lungs. Transient overexpression of catalytically inactive PKCδ cDNA in the endothelium significantly attenuated LPS-induced endothelial barrier dysfunction in vitro and increased k(f) lung values in PKCδ(+/+) mice. However, transient overexpression of wild-type PKCδ cDNA in PKCδ(-/-) mouse lung vasculature did not alter the protective effects of PKCδ deficiency against LPS-induced acute lung injury. We conclude that PKCδ plays a role in the pathological progression of endotoxin-induced lung injury, likely mediated through modulation of inflammatory signaling and pulmonary vascular barrier function."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.org/dc/terms/identifier | "doi:10.1152/ajplung.00169.2012"xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Chung C.S."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Ayala A."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Klinger J.R."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Harrington E.O."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Rounds S."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Lomas-Neira J."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Chichger H."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Grinnell K.L."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Casserly B."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/author | "Braza J."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/name | "Am J Physiol Lung Cell Mol Physiol"xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/pages | "L880-8"xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/title | "Genetic disruption of protein kinase Cdelta reduces endotoxin-induced lung injury."xsd:string |
http://purl.uniprot.org/citations/22983354 | http://purl.uniprot.org/core/volume | "303"xsd:string |
http://purl.uniprot.org/citations/22983354 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22983354 |
http://purl.uniprot.org/citations/22983354 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/22983354 |
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