ArticlePediatric pulmonology2016
Perinatal nicotine exposure induces myogenic differentiation, but not epithelial-mesenchymal transition in rat offspring lung.
Article in Pediatric pulmonology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Past as Prologue: Vaping Effects on the Developing Lung.American journal of respiratory cell and molecular biology · 2020Article
- Prenatal Exposure to Electronic-Cigarette Aerosols Leads to Sex-Dependent Pulmonary Extracellular-Matrix Remodeling and Myogenesis in Offspring Mice.American journal of respiratory cell and molecular biology · 2020Article
- Antenatal PPAR-γ agonist pioglitazone stimulates fetal lung maturation equally in males and females.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Mechanism underlying increased cardiac extracellular matrix deposition in perinatal nicotine-exposed offspring.American journal of physiology. Heart and circulatory physiology · 2020Article
- Inhaled vitamin A is more effective than intramuscular dosing in mitigating hyperoxia-induced lung injury in a neonatal rat model of bronchopulmonary dysplasia.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Comparison of Protective Effects of Electroacupuncture at ST 36 and LU 5 on Pulmonary and Hypothalamic Pituitary Adrenal Axis Changes in Perinatal Nicotine-Exposed Rats.BioMed research international · 2020Article
- Pediatric pulmonology year in review 2016: Part 2.Pediatric pulmonology · 2017Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
objectivePerinatal nicotine exposure alters offspring lung structure and function; however, the underlying mechanisms remain incompletely understood. Whether epithelial-mesenchymal transition (EMT), a known contributor to pulmonary pathology, occurs following moderate perinatal nicotine exposure is not known.
methodsPregnant, pair-fed Sprague Dawley rat dams received either placebo (diluent) or nicotine [1 mg/kg, subcutaneously] once daily from embryonic day (e) 6 to postnatal day (PND) 21. Generation 1 (F1) and 3 (F3) offspring lungs were isolated at PND 21, and using Western analysis, q-RT-PCR and immunohistochemistry examined for evidence of EMT. To gain further supportive evidence for nicotine-induced EMT, embryonic day 19 primary rat lung alveolar type II (ATII) cells were cultured and treated with nicotine for 24 hr.
resultsProtein levels of α-smooth muscle actin, fibronectin, and calponin (myogenic differentiation markers) increased significantly. However, surfactant proteins B and C, and cholinephosphate cytidylyltransferase-α (epithelial cell markers), as well as the typical markers of EMT, E-cadherin, N-cadherin, and fibroblast specific protein (FSP)-1, in both F1 and F3 generation lungs, showed no significant change between the nicotine exposed and control dams. Immunostaining of lung sections and data from in vitro treated ATII cells strongly supported the Western data.
conclusionsEnhanced myogenic molecular profile, without evidence of EMT, as evidenced by the absence of the loss of E-cadherin or gains in N-cadherin and FSP-1, suggest that perinatal nicotine exposure does not result in EMT, but it leads to myogenesis, which predominantly accounts for the lung phenotype seen in perinatally nicotine exposed rat offspring. Pediatr Pulmonol. 2016;51:1142-1150. © 2016 Wiley Periodicals, Inc.
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