ArticleToxicology and applied pharmacology2008
Regulation of caveolin-1 expression, nitric oxide production and tissue injury by tumor necrosis factor-alpha following ozone inhalation.
Article in Toxicology and applied pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Role of PPARγ in dyslipidemia and altered pulmonary functioning in mice following ozone exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Ozone-induced changes in the murine lung extracellular vesicle small RNA landscape.Physiological reports · 2021Article
- The Potential Contribution of Caveolin 1 to HIV Latent Infection.Pathogens (Basel, Switzerland) · 2020Review
- Regulation of Lung Macrophage Activation and Oxidative Stress Following Ozone Exposure by Farnesoid X Receptor.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- Effects and mechanisms of pirfenidone, prednisone and acetylcysteine on pulmonary fibrosis in rat idiopathic pulmonary fibrosis models.Pharmaceutical biology · 2017Article
- Anti-TNFα therapy in inflammatory lung diseases.Pharmacology & therapeutics · 2017Review
- 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
- Decreased Expression of Caveolin-1 Contributes to the Pathogenesis of Psoriasiform Dermatitis in Mice.The Journal of investigative dermatology · 2015Article
- Ozone-induced lung injury and sterile inflammation. Role of toll-like receptor 4.Experimental and molecular pathology · 2012Article
- Role of TNFR1 in lung injury and altered lung function induced by the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide.Toxicology and applied pharmacology · 2011Article
- New glimpses of caveolin-1 functions in embryonic development and human diseases.Frontiers in biology · 2011Review
- Macrophages and tissue injury: agents of defense or destruction?Annual review of pharmacology and toxicology · 2011Review
- Macrophages, reactive nitrogen species, and lung injury.Annals of the New York Academy of Sciences · 2010Review
- Caveolin-1 regulates leucocyte behaviour in fibrotic lung disease.Annals of the rheumatic diseases · 2010Article
- Article
- Potential role of caveolin-1 in acetaminophen-induced hepatotoxicity.Toxicology and applied pharmacology · 2010Article
- Enhanced death signaling in ozone-exposed ischemic-reperfused hearts.Molecular and cellular biochemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Alveolar macrophages (AM) and inflammatory mediators including nitric oxide and peroxynitrite contribute to ozone-induced lung injury. The generation of these mediators is regulated, in part, by the transcription factor NF-kappaB. We previously demonstrated a critical role for NF-kappaB p50 in ozone-induced injury. In the present studies mechanisms regulating NF-kappaB activation in the lung after ozone inhalation were analyzed. Treatment of wild type (WT) mice with ozone (0.8 ppm, 3 h) resulted in a rapid increase in NF-kappaB binding activity in AM, which persisted for at least 12 h. This was not evident in mice lacking TNFalpha which are protected from ozone-induced injury; there was also no evidence of nitric oxide or peroxynitrite production in lungs from these animals. These data demonstrate that TNFalpha plays a role in NF-kappaB activation and toxicity. TNFalpha signaling involves PI-3-kinase (PI3K)/protein kinase B (PKB), and p44/42 MAP kinase (MAPK) which are important in NF-kappaB activation. Ozone Inhalation resulted in rapid and transient increases in p44/42 MAPK and PI3K/PKB in AM from WT mice, which was evident immediately after exposure. Caveolin-1, a transmembrane protein that negatively regulates PI3K/PKB and p44/42 MAPK signaling, was downregulated in AM from WT mice after ozone exposure. In contrast, ozone had no effect on caveolin-1, PI3K/PKB or p44/42 MAPK expression in AM from TNFalpha knockout mice. These data, together with our findings that TNFalpha suppressed caveolin-1 expression in cultured AM, suggest that TNFalpha and downstream signaling mediate activation of NF-kappaB and the regulation of inflammatory genes important in ozone toxicity, and that this process is linked to caveolin-1.
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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.