ArticleEnvironmental health perspectives2015
Novel Roles for Notch3 and Notch4 Receptors in Gene Expression and Susceptibility to Ozone-Induced Lung Inflammation in Mice.
Article in Environmental health perspectives, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Prenatal Particulate Air Pollution and DNA Methylation in Newborns: An Epigenome-Wide Meta-Analysis.Environmental health perspectives · 2019Pooled it
- Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury.American journal of respiratory cell and molecular biology · 2017Pooled it
- Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice.American journal of physiology. Lung cellular and molecular physiology · 2026Article
- Article
- Exploring Protein Functions of Gut Bacteriome and Mycobiome in Thai Infants Associated with Atopic Dermatitis Through Metaproteomic and Host Interaction Analysis.International journal of molecular sciences · 2024Article
- 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
- Assemblies of JAG1 and JAG2 determine tracheobronchial cell fate in mucosecretory lung disease.JCI insight · 2022Article
- Compartment-specific transcriptomics of ozone-exposed murine lungs reveals sex- and cell type-associated perturbations relevant to mucoinflammatory lung diseases.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- NOTCH4 Exhibits Anti-Inflammatory Activity in Activated Macrophages by Interfering With Interferon-γ and TLR4 Signaling.Frontiers in immunology · 2021Article
- Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Sex Modifies Acute Ozone-Mediated Airway Physiologic Responses.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Newly divided eosinophils limit ozone-induced airway hyperreactivity in nonsensitized guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Effects of mannose-binding lectin on pulmonary gene expression and innate immune inflammatory response to ozone.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Loss of Activin Receptor Type 1B Accelerates Development of Intraductal Papillary Mucinous Neoplasms in Mice With Activated KRAS.Gastroenterology · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOzone is a highly toxic air pollutant and global health concern. Mechanisms of genetic susceptibility to ozone-induced lung inflammation are not completely understood. We hypothesized that Notch3 and Notch4 are important determinants of susceptibility to ozone-induced lung inflammation.
methodsWild-type (WT), Notch3 (Notch3-/-), and Notch4 (Notch4-/-) knockout mice were exposed to ozone (0.3 ppm) or filtered air for 6-72 hr.
resultsRelative to air-exposed controls, ozone increased bronchoalveolar lavage fluid (BALF) protein, a marker of lung permeability, in all genotypes, but significantly greater concentrations were found in Notch4-/- compared with WT and Notch3-/- mice. Significantly greater mean numbers of BALF neutrophils were found in Notch3-/- and Notch4-/- mice compared with WT mice after ozone exposure. Expression of whole lung Tnf was significantly increased after ozone in Notch3-/- and Notch4-/- mice, and was significantly greater in Notch3-/- compared with WT mice. Statistical analyses of the transcriptome identified differentially expressed gene networks between WT and knockout mice basally and after ozone, and included Trim30, a member of the inflammasome pathway, and Traf6, an inflammatory signaling member.
conclusionsThese novel findings are consistent with Notch3 and Notch4 as susceptibility genes for ozone-induced lung injury, and suggest that Notch receptors protect against innate immune inflammation.
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