ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Genetic disruption of protein kinase Cδ reduces endotoxin-induced lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- T1R3 Anchors ACE2 at the Pulmonary Endothelial Cell Surface to Attenuate Vascular Injury Following SARS-CoV-2 Spike 1 Protein Exposure In Vitro.Journal of cellular and molecular medicine · 2026Article
- Plasma Lipidomics Identify Pathways Linked to Acute Lung Injury in a Porcine One-Lung Ventilation Surgery Model.International journal of molecular sciences · 2026Article
- Article
- Knockout of PKC θ gene attenuates oleic acid-induced acute lung injury via reduction of inflammation and oxidative stress.Iranian journal of basic medical sciences · 2021Article
- Functional proteomic analysis reveals roles for PKCδ in regulation of cell survival and cell death: Implications for cancer pathogenesis and therapy.Advances in biological regulation · 2020Article
- Protein kinase C-delta inhibition is organ-protective, enhances pathogen clearance, and improves survival in sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Protein Kinase C-Delta (PKCδ) Tyrosine Phosphorylation is a Critical Regulator of Neutrophil-Endothelial Cell Interaction in Inflammation.Shock (Augusta, Ga.) · 2019Article
- The Role of Tyrosine Phosphorylation of Protein Kinase C Delta in Infection and Inflammation.International journal of molecular sciences · 2019Review
- Activation of the sweet taste receptor, T1R3, by the artificial sweetener sucralose regulates the pulmonary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Multifunctional roles of PKCδ: Opportunities for targeted therapy in human disease.Pharmacology & therapeutics · 2016Review
- Select Rab GTPases Regulate the Pulmonary Endothelium via Endosomal Trafficking of Vascular Endothelial-Cadherin.American journal of respiratory cell and molecular biology · 2016Article
- Regulation of Thrombin-Induced Lung Endothelial Cell Barrier Disruption by Protein Kinase C Delta.PloS one · 2016Article
- Biodistribution and Efficacy of Targeted Pulmonary Delivery of a Protein Kinase C-δ Inhibitory Peptide: Impact on Indirect Lung Injury.The Journal of pharmacology and experimental therapeutics · 2015Article
- Involvement of Protein Kinase C-δ in Vascular Permeability in Acute Lung Injury.Immune network · 2015Article
- Lysophosphatidic acid receptor 1 antagonist ki16425 blunts abdominal and systemic inflammation in a mouse model of peritoneal sepsis.Translational research : the journal of laboratory and clinical medicine · 2015Article
- SH2 domain-containing protein tyrosine phosphatase 2 and focal adhesion kinase protein interactions regulate pulmonary endothelium barrier function.American journal of respiratory cell and molecular biology · 2015Article
- p18, a novel adaptor protein, regulates pulmonary endothelial barrier function via enhanced endocytic recycling of VE-cadherin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Article
- Protein kinase Cδ protects against bile acid apoptosis by suppressing proapoptotic JNK and BIM pathways in human and rat hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Novel regulators of endothelial barrier function.American journal of physiology. Lung cellular and molecular physiology · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
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