ArticleAmerican journal of respiratory and critical care medicine2007
Signal transduction pathways of tumor necrosis factor--mediated lung injury induced by ozone in mice.
Article in American journal of respiratory and critical care medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 92 citations in OpenAlex.
- Hyaluronan Signaling Ameliorates the Epithelial Injury Response and Barrier Disruption After Ozone Exposure.Biomolecules · 2026Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Overexpression of endothelial S1pr2 promotes blood-brain barrier disruption via JNK/c-Jun/MMP-9 pathway after traumatic brain injury in bothFrontiers in pharmacology · 2024Article
- Multi-Omics Analysis of Lung Tissue Demonstrates Changes to Lipid Metabolism during Allergic Sensitization in Mice.Metabolites · 2023Article
- The relationship among air pollution, meteorological factors and COVID-19 in the Brussels Capital Region.The Science of the total environment · 2023Article
- Selenium-Containing Compound Ameliorates Lipopolysaccharide-Induced Acute Lung Injury via Regulating the MAPK/AP-1 Pathway.Inflammation · 2021Article
- Murine Neonatal Oxidant Lung Injury: NRF2-Dependent Predisposition to Adulthood Respiratory Viral Infection and Protection by Maternal Antioxidant.Antioxidants (Basel, Switzerland) · 2021Article
- Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Role for Mucin-5AC in Upper and Lower Airway Pathogenesis in Mice.Toxicologic pathology · 2021Article
- Effect of water-soluble PMJournal of environmental health science & engineering · 2021Article
- Understanding the Functional Impact of VOC-Ozone Mixtures on the Chemistry of RNA in Epithelial Lung Cells.Research report (Health Effects Institute) · 2020Article
- Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?Environmental pollution (Barking, Essex : 1987) · 2020Article
- Isoprostanes as Biomarker for White Matter Injury in Extremely Preterm Infants.Frontiers in pediatrics · 2020Article
- Article
- Major Effect of Oxidative Stress on the Male, but Not Female, SP-A1 Type II Cell miRNome.Frontiers in immunology · 2019Article
- SP-A2 contributes to miRNA-mediated sex differences in response to oxidative stress: pro-inflammatory, anti-apoptotic, and anti-oxidant pathways are involved.Biology of sex differences · 2017Article
- Anti-TNFα therapy in inflammatory lung diseases.Pharmacology & therapeutics · 2017Review
- Protective Role of Eosinophils and TNFa after Ozone Inhalation.Research report (Health Effects Institute) · 2017Article
- Editor's Highlight: CCR2 Regulates Inflammatory Cell Accumulation in the Lung and Tissue Injury following Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
rationaleIncreasing evidence suggests that tumor necrosis factor (TNF)-alpha plays a key role in pulmonary injury caused by environmental ozone (O(3)) in animal models and human subjects. We previously determined that mice genetically deficient in TNF response are protected from lung inflammation and epithelial injury after O(3) exposure.
objectivesThe present study was designed to determine the molecular mechanisms of TNF receptor (TNF-R)-mediated lung injury induced by O(3).
methodsTNF-R knockout (Tnfr(-/-)) and wild-type (Tnfr(+/+)) mice were exposed to 0.3 ppm O(3) or air (for 6, 24, or 48 h), and lung RNA and proteins were prepared. Mice deficient in p50 nuclear factor (NF)-kappaB (Nfkb1(-/-)) or c-Jun-NH(2) terminal kinase 1 (Jnk1(-/-)) and wild-type controls (Nfkb1(+/+), Jnk1(+/+)) were exposed to O(3) (48 h), and the role of NF-kappaB and mitogen-activated protein kinase (MAPK) as downstream effectors of lung injury was analyzed by bronchoalveolar lavage analyses.
resultsO(3)-induced early activation of TNF-R adaptor complex formation was attenuated in Tnfr(-/-) mice compared with Tnfr(+/+) mice. O(3) significantly activated lung NF-kappaB in Tnfr(+/+) mice before the development of lung injury. Basal and O(3)-induced NF-kappaB activity was suppressed in Tnfr(-/-) mice. Compared with Tnfr(+/+) mice, MAPKs and activator protein (AP)-1 were lower in Tnfr(-/-) mice basally and after O(3). Furthermore, inflammatory cytokines, including macrophage inflammatory protein-2, were differentially expressed in Tnfr(-/-) and Tnfr(+/+) mice after O(3). O(3)-induced lung injury was significantly reduced in Nfkb1(-/-) and Jnk1(-/-) mice relative to respective control animals.
conclusionsResults suggest that NF-kappaB and MAPK/AP-1 signaling pathways are essential in TNF-R-mediated pulmonary toxicity induced by O(3).
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Registered trials
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