ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
PPARγ agonist rosiglitazone prevents perinatal nicotine exposure-induced asthma in rat offspring.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. 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, 51 citations in OpenAlex.
- Perinatal nicotine vaping exposure induces pro-myofibroblastic phenotype in rat bone marrow-derived mesenchymal stem cells.Reproductive toxicology (Elmsford, N.Y.) · 2024Article
- Perinatal Exposure to Nicotine Alters Sperm RNA Profiles in Rats.Frontiers in endocrinology · 2022Article
- Antenatal PPAR-γ agonist pioglitazone stimulates fetal lung maturation equally in males and females.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Developmental Timing Determines the Protective Effect of Maternal Electroacupuncture on Perinatal Nicotine Exposure-Induced Offspring Lung Phenotype.BioMed research international · 2020Article
- Epigenetic impacts of maternal tobacco and e-vapour exposure on the offspring lung.Clinical epigenetics · 2019Review
- Prevention of perinatal nicotine-induced bone marrow mesenchymal stem cell myofibroblast differentiation by augmenting the lipofibroblast phenotype.Clinical science (London, England : 1979) · 2018Article
- Article
- The Role of Nicotine in the Effects of Maternal Smoking during Pregnancy on Lung Development and Childhood Respiratory Disease. Implications for Dangers of E-Cigarettes.American journal of respiratory and critical care medicine · 2016Article
- PPAR-γ agonist rosiglitazone reverses perinatal nicotine exposure-induced asthma in rat offspring.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Perinatal nicotine exposure suppresses PPARγ epigenetically in lung alveolar interstitial fibroblasts.Molecular genetics and metabolism · 2015Article
- The PPARγ agonist, rosiglitazone, attenuates airway inflammation and remodeling via heme oxygenase-1 in murine model of asthma.Acta pharmacologica Sinica · 2015Article
- Inter- and transgenerational epigenetic inheritance: evidence in asthma and COPD?Clinical epigenetics · 2015Article
- The lung alveolar lipofibroblast: an evolutionary strategy against neonatal hyperoxic lung injury.Antioxidants & redox signaling · 2014Review
- The electronic cigarette: a knight in shining armour or a Trojan horse?Psychiatric bulletin (2014) · 2014Article
- Nicotine stimulates nerve growth factor in lung fibroblasts through an NFκB-dependent mechanism.PloS one · 2014Article
- Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013Review
- Perinatal nicotine-induced transgenerational asthma.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Sex-specific perinatal nicotine-induced asthma in rat offspring.American journal of respiratory cell and molecular biology · 2013Article
- Perinatal nicotine exposure induces asthma in second generation offspring.BMC medicine · 2012Article
- Prenatal nicotine exposure alters lung function and airway geometry through α7 nicotinic receptors.American journal of respiratory cell and molecular biology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Perinatal exposure to maternal smoke is associated with adverse pulmonary effects, including reduced lung function and increased incidence of asthma. However, the mechanisms underlying these effects are unknown, and there is no effective preventive and/or therapeutic intervention. Recently, we suggested that downregulation of homeostatic mesenchymal peroxisome proliferator-activated receptor-γ (PPARγ) signaling following in utero nicotine exposure might contribute to chronic lung diseases such as asthma. We used an in vivo rat model to determine the effect of perinatal nicotine exposure on 1) offspring pulmonary function, 2) mesenchymal markers of airway contractility in trachea and lung tissue, and 3) whether administration of a PPARγ agonist, rosiglitazone (RGZ), blocks the molecular and functional effects of perinatal nicotine exposure on offspring lung. Pregnant Sprague-Dawley rat dams received placebo, nicotine, or nicotine + RGZ daily from embryonic day 6 until postnatal day 21, when respiratory system resistance, compliance, tracheal contractility, and the expression of markers of pulmonary contractility were determined. A significant increase in resistance and a decrease in compliance under basal conditions, with more pronounced changes following methacholine challenge, were observed with perinatal nicotine exposure compared with control. Tracheal constriction response and expression of mesenchymal markers of airway contractility were also significantly increased following perinatal nicotine exposure. Concomitant treatment with RGZ completely blocked the nicotine-induced alterations in pulmonary function, as well as the markers of airway contractility, at proximal and distal airway levels. These data suggest that perinatal smoke exposure-induced asthma can be effectively blocked by PPARγ agonists.
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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.