ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Endothelial cell peroxisome proliferator-activated receptor γ reduces endotoxemic pulmonary inflammation and injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Necrotizing enterocolitis in premature infants-A defect in the brakes? Evidence from clinical and animal studies.Mucosal immunology · 2023Review
- Nitro-oleic acid regulates T cell activation through post-translational modification of calcineurin.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Systemic and Airway Epigenetic Disruptions Are Associated with Health Status in COPD.Biomedicines · 2023Article
- Dietary administration of the glycolytic inhibitor 2-deoxy-D-glucose reduces endotoxemia-induced inflammation and oxidative stress: Implications in PAMP-associated acute and chronic pathology.Frontiers in pharmacology · 2023Article
- MicroRNA 573 Rescues Endothelial Dysfunction during Dengue Virus Infection under PPARγ Regulation.Journal of virology · 2022Article
- Important Functions and Molecular Mechanisms of Mitochondrial Redox Signaling in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2022Review
- Effects of fatty acid nitroalkanes on signal transduction pathways and airway macrophage activation.Innate immunity · 2021Article
- Chronic Low-Dose Alcohol Consumption Attenuates Post-Ischemic Inflammation via PPARγ in Mice.International journal of molecular sciences · 2021Article
- Targeting inflammatory cytokine storm to fight against COVID-19 associated severe complications.Life sciences · 2021Review
- PPAR Gamma: From Definition to Molecular Targets and Therapy of Lung Diseases.International journal of molecular sciences · 2021Review
- Fatty acid nitroalkenes inhibit the inflammatory response to bleomycin-mediated lung injury.Toxicology and applied pharmacology · 2020Article
- Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Redox Biology of Peroxisome Proliferator-Activated Receptor-γ in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Electrophiles modulate glutathione reductase activity via alkylation and upregulation of glutathione biosynthesis.Redox biology · 2019Article
- Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Nitrolipids in kidney physiology and disease.Nitric oxide : biology and chemistry · 2018Review
- Hypaphorine Attenuates Lipopolysaccharide-Induced Endothelial Inflammation via Regulation of TLR4 and PPAR-γ Dependent on PI3K/Akt/mTOR Signal Pathway.International journal of molecular sciences · 2017Article
- PPAR Agonists for the Prevention and Treatment of Lung Cancer.PPAR research · 2017Review
- PPARγ signaling and emerging opportunities for improved therapeutics.Pharmacological research · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bacterial endotoxin (LPS)-mediated sepsis involves severe, dysregulated inflammation that injures the lungs and other organs, often fatally. Vascular endothelial cells are both key mediators and targets of LPS-induced inflammatory responses. The nuclear hormone receptor peroxisome proliferator-activated receptor γ (PPARγ) exerts anti-inflammatory actions in various cells, but it is unknown whether it modulates inflammation through actions within endothelial cells. To determine whether PPARγ acts within endothelial cells to diminish endotoxemic lung inflammation and injury, we measured inflammatory responses and mediators in mice with endothelial-targeted deletion of PPARγ. Endothelial cell PPARγ (ePPARγ) knockout exacerbated LPS-induced pulmonary inflammation and injury as shown by several measures, including infiltration of inflammatory cells, edema, and production of reactive oxygen species and proinflammatory cytokines, along with upregulation of the LPS receptor TLR4 in lung tissue and increased activation of its downstream signaling pathways. In isolated LPS-stimulated endothelial cells in vitro, absence of PPARγ enhanced the production of numerous inflammatory markers. We hypothesized that the observed in vivo activity of the ligand-activated ePPARγ may arise, in part, from nitrated fatty acids (NFAs), a novel class of endogenous PPARγ ligands. Supporting this idea, we found that treating isolated endothelial cells with physiologically relevant concentrations of the endogenous NFA 10-nitro-oleate reduced LPS-induced expression of a wide range of inflammatory markers in the presence of PPARγ, but not in its absence, and also inhibited neutrophil mobility in a PPARγ-dependent manner. Our results demonstrate a key protective role of ePPARγ against endotoxemic injury and a potential ePPARγ-mediated anti-inflammatory role for NFAs.
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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.