Newborn Mice Lacking the Gene for Cyp1a1 Are More Susceptible to Oxygen-Mediated Lung Injury, and Are Rescued by Postnatal β-Naphthoflavone Administration: Implications for Bronchopulmonary Dysplasia in Premature Infants
Author:
Affiliation:
1. Section of Neonatology, Department of Pediatrics, Texas Children’s Hospital, Baylor College of Medicine, Houston, Texas 77030;
2. Department of Pathology and Genomic Medicine, The Methodist Hospital Physician Organization, Houston, Texas 77030
Funder
National Institutes of Health
Publisher
Oxford University Press (OUP)
Subject
Toxicology
Link
http://academic.oup.com/toxsci/article-pdf/157/1/260/24194923/kfx036.pdf
Reference54 articles.
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2. Animal models of bronchopulmonary dysplasia. The term mouse models;Berger;Am. J. Physiol. Lung Cell. Mol. Physiol,2014
3. BPD following preterm birth: A model for chronic lung disease and a substrate for ARDS in childhood;Bhandari;Front. Pediatr,2016
4. Induction of expression of aryl hydrocarbon receptor-dependent genes in human HepaRG cell line modified by shRNA and treated with beta-naphthoflavone;Brauze;Mol. Cell. Biochem,2017
5. The murine Cyp1a1 gene is expressed in a restricted spatial and temporal pattern during embryonic development;Campbell;J. Biol. Chem,2005
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5. Correction to: Newborn Mice Lacking the Gene for Cyp1a1 Are More Susceptible to Oxygen-Mediated Lung Injury, and Are Rescued by Postnatal β-Naphthoflavone Administration: Implications for Bronchopulmonary Dysplasia in Premature Infants;Toxicological Sciences;2022-03-26
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