ArticleJournal of leukocyte biology2011
Protection against sepsis-induced lung injury by selective inhibition of protein kinase C-δ (δ-PKC).
Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Protein Kinase C-Delta (PKCδ) inhibition stabilizes endothelium and suppresses triple-negative breast cancer (TNBC) intravasation in a microfluidic hypoxic tumor model.Bioengineering & translational medicine · 2026Article
- The macrophage DAG/PKCα/ROS axis exacerbates sepsis by inducing endothelial dysfunction through activation of the p38 MAPK pathway.Molecular biology reports · 2026Article
- FTO-mediated demethylation of PRKCB mRNA activates NF-κB to trigger alveolar fibrin deposition in ARDS.Frontiers in immunology · 2026Article
- Endothelial Poldip2 regulates sepsis-induced lung injury via Rho pathway activation.Cardiovascular research · 2022Article
- lncRNA IL-17RA-1 Attenuates LPS-Induced Sepsis via miR-7847-3p/PRKCG-Mediated MAPK Signaling Pathway.Mediators of inflammation · 2022Article
- Emerging Approaches to Understanding Microvascular Endothelial Heterogeneity: A Roadmap for Developing Anti-Inflammatory Therapeutics.International journal of molecular sciences · 2021Review
- 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
- Signal Transduction in Immune Cells and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Experimental Approaches to Evaluate Leukocyte-Endothelial Cell Interactions in Sepsis and Inflammation.Shock (Augusta, Ga.) · 2020Article
- Diallyl Trisulfide (DATS) Suppresses AGE-Induced Cardiomyocyte Apoptosis by Targeting ROS-Mediated PKCδ Activation.International journal of molecular sciences · 2020Article
- Neutrophil-endothelial interactions of murine cells is not a good predictor of their interactions in human cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 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
- Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions.International journal of molecular sciences · 2020Article
- A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS).International journal of molecular sciences · 2019Article
- 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
- Protein kinase C-delta inhibition protects blood-brain barrier from sepsis-induced vascular damage.Journal of neuroinflammation · 2018Article
- Role of Protein Kinase C-delta in regulating platelet activation and platelet-leukocyte interaction during sepsis.PloS one · 2018Article
- PKC-δ isoform plays a crucial role in Tat-TLR4 signalling pathway to activate NF-κB and CXCL8 production.Scientific reports · 2017Article
- A novel microfluidic assay reveals a key role for protein kinase C δ in regulating human neutrophil-endothelium interaction.Journal of leukocyte biology · 2016Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation and proinflammatory mediators are activators of δ-PKC. In vitro, δ-PKC regulates proinflammatory signaling in neutrophils and endothelial and epithelial cells, cells that can contribute to lung tissue damage associated with inflammation. In this study, a specific δ-PKC TAT peptide inhibitor was used to test the hypothesis that inhibition of δ-PKC would attenuate lung injury in an animal model of ARDS. Experimental ARDS was induced in rats via 2CLP, a model of polymicrobial sepsis. Following 2CLP surgery, the δ-PKC TAT inhibitory peptide (2CLP+δ-PKC TAT in PBS) or PBS (2CLP+PBS) was administered intratracheally. Controls consisted of SO, where animals underwent a laparotomy without 2CLP. Twenty-four hours after SO or 2CLP, blood, BALF, and lung tissue were collected. 2CLP induced δ-PKC phosphorylation in the lung within 24 h. Treatment with the δ-PKC TAT inhibitory peptide significantly decreased pulmonary δ-PKC phosphorylation, indicating effective inhibition of δ-PKC activation. Plasma and BALF levels of the chemokines CINC-1 and MIP-2 were elevated in 2CLP + PBS rats as compared with SO rats. Treatment with δ-PKC TAT reduced 2CLP-induced elevations in chemokine levels in BALF and plasma, suggesting that δ-PKC modulated chemokine expression. Most importantly, intratracheal administration of δ-PKC TAT peptide significantly attenuated inflammatory cell infiltration, disruption of lung architecture, and pulmonary edema associated with 2CLP. Thus, δ-PKC is an important regulator of proinflammatory events in the lung. Targeted inhibition of δ-PKC exerted a lung-protective effect 24 h after 2CLP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.