Fetal and Neonatal Exposure to Nicotine Disrupts Postnatal Lung Development in Rats: Role of VEGF and Its Receptors

Petre, Maria A.; Petrik, Jim; Ellis, Russ; Inman, Mark D.; Holloway, Alison C.; Labiris, N. R.

doi:10.1177/1091581810395332

Cited by 30 publications

(38 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings suggest that lungs recover from acute lung injury in a continuing environment of moderate hyperoxia for a further 2 weeks. Structural changes were similar to those examined in previous literature, such as increased alveolar volume, decreased internal surface area and increased airway wall area [5,14,15]. Given that early abnormal lung development may predispose people to respiratory disease in later life [16], these results suggest that fetal and neonatal nicotine exposure may inhibit alveolarization and adversely affect respiratory outcomes in children born to mothers who smoke during pregnancy and infancy.…”

Section: Discussionsupporting

confidence: 70%

Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats

Huang

Chou²,

Lin³

et al. 2014

Neonatology

View full text Add to dashboard Cite

Background: Maternal nicotine exposure increases lung collagen in fetal and newborn animals. Connective tissue growth factor (CTGF) plays a role in hyperoxia-induced pulmonary fibrosis. Objective: To determine whether pre- and postnatal nicotine exposure can augment CTGF expression and postnatal hyperoxia-induced lung fibrosis. Methods: Nicotine was administered to pregnant Sprague-Dawley rats at a dose of 6 mg/kg/day from gestational days 7-21 (prenatal nicotine-treated group) and gestational day 7 to postnatal day 14 (pre- and postnatal nicotine-treated group). A control group of pregnant dams was injected with an equal volume of saline. Within 12 h of birth, rats were exposed to room air or 1 week of >95% O₂ and an additional 2 weeks of 60% O₂ (3 weeks of hyperoxia). Lungs were taken for total collagen, CTGF expression and histological analyses. Results: In each maternal treatment group, the rats reared in hyperoxia had a higher total collagen compared with rats reared in room air on postnatal days 7 and 21. Collagen content was significantly higher in rats born to pre- and postnatal nicotine-treated dams than rats born to saline-treated and prenatal nicotine-treated dams on postnatal days 7 and 21. Pre- and postnatal nicotine exposure and neonatal hyperoxia exposure increased CTGF expression on postnatal days 7 and 21. Conclusions: CTGF may be involved in the pathogenesis of lung fibrosis induced by maternal nicotine and neonatal hyperoxia, and maternal nicotine exposure exacerbates neonatal hyperoxia-induced lung fibrosis. These results are relevant to neonates who require supplemental oxygen and are exposed to the breast milk of smoking mothers during infancy.

show abstract

Section: Discussionsupporting

confidence: 70%

Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats

Huang

Chou²,

Lin³

et al. 2014

Neonatology

View full text Add to dashboard Cite

show abstract

“…Tobacco smoking during pregnancy remains common and many women are unable to quit smoking during pregnancy [2]. Children of smoking mothers have an increased risk of developing asthma, bronchitis, and respiratory illness later in life for reasons that remain largely unknown [3,4].…”

Section: Introductionmentioning

confidence: 99%

Effects of perinatal nicotine exposure on the development of albino rat’s alveoli with special reference to the role of the vascular endothelial growth factor

Ibrahim

Selim²

2012

The Egyptian Journal of Histology

View full text Add to dashboard Cite

BackgroundNicotine is one of the most toxic and addictive agents in cigarette smoke. Maternal cigarette smoking may affect lung development and maturation of the fetus. Recently, it has been reported that blood vessels promote alveolar growth during development and contribute toward the maintenance of alveolar structures throughout postnatal life. Aim of the workThe aims of this study were to determine the effects of perinatal nicotine exposure on the histological structures of the developing alveoli of offspring with special reference to the role of vascular endothelial growth factors (VEGF). Materials and methodsTen healthy pregnant rats were divided equally into control (I) and treated (II) groups. Rats of group II were subjected to a daily subcutaneous injection of 1 mg/kg of nicotine from the seventh day of gestation until the end of the experiment. Their offspring were subdivided into two subgroups at 2 and 21 postnatal days. At the time of sacrifice, all rats were anesthetized with ether and lung samples were processed for light and electron microscopic examination. Also, an immunohistochemical study was carried out for VEGF. The alveolar diameter, thickening of interalveolar septa, number of vacuolated interstitial cells, and the surface area of VEGF immunoexpression were determined and analyzed statistically. ResultsIn the nicotine-exposed groups, widening in alveoli and thinning of interalveolar septa in the offspring were observed. Also, the same offspring showed a reduction in VEGF immunoexpression. All these results were confirmed statistically especially at 3 weeks of age or at the time of weaning. Also, swelling in pneumocyte type I and deformed blood air barriers with a subsequent statistical increase in the number of vacuolated interstitial cells (pneumocyte type II) were observed. ConclusionIn the current work, it was found that perinatal exposure to nicotine altered lung development, an effect that may be mediated by decreased VEGF. Thus, avoidance of maternal smoking during pregnancy and lactation is highly recommended.

show abstract

“…Importantly, approximately 12-22 % of women smoke during pregnancy [82][83][84][85][86][87]. Data from animal studies and observations in humans show that smoking during pregnancy is associated with lower lung function in offspring and increases in airway smooth muscle, decreasing alveolar surface area and collagen deposition [78,79,88,89]. Effects influencing lung function such as these can be attributable to epigenetic changes which may lead to a predisposition to developing COPD.…”

Section: Epigenetics Considerations In Lung Function and Copdmentioning

confidence: 99%

“…Furthermore, maternal smoking has been demonstrated to be associated with lower adult lung volume independent to post-natal exposure and of personal smoking [72][73][74][75][76]. Of the wide range of components in tobacco smoke nicotine is thought to be the key component which alters lung development, principally because it is easily transferred to the foetus in utero in circulating blood [77][78][79][80][81]. Importantly, approximately 12-22 % of women smoke during pregnancy [82][83][84][85][86][87].…”

Section: Epigenetics Considerations In Lung Function and Copdmentioning

confidence: 99%

Developmental genetics of the COPD lung

et al. 2015

View full text Add to dashboard Cite

Chronic Obstructive Pulmonary Disease (COPD) is a debilitating disease of the lung which results in irreversible airflow obstruction and is currently the third leading cause of death worldwide. Genetic and environmental factors contributing to COPD are presently under investigation. As lung function measures cluster within families, we now know that lung function is partly inherited. Thus, identifying genes involved in determining lung function at the population level and in determining the risk of development of COPD is important. A thorough understanding of the mechanisms underlying maintenance of lung function and knowledge of how these are altered in lung disease could ultimately lead to targeted therapeutic approaches. This is of potential value in COPD because current treatments are designed to reduce symptoms but do not modify disease progression. Here, we review the genes identified from both meta-analyses of genome-wide association (GWA) studies of lung function in large populations and case control GWA studies in COPD. We hypothesise that mechanisms involved in the early development of the lungs may vary/alter and predispose to COPD later in life. We discuss the genes and pathways involved in normal lung development and ascertain whether they overlap with key genes identified from GWA studies. Epigenetic factors may also play an important role in lung function, development and disease. Furthermore, we discuss our findings on the functional characterisation of HTR4 and genes within the 4q24 locus associated with both lung function and COPD. Lastly, we consider new genetic techniques and models to study candidate genes identified by the approaches discussed.

show abstract

Fetal and Neonatal Exposure to Nicotine Disrupts Postnatal Lung Development in Rats: Role of VEGF and Its Receptors

Cited by 30 publications

References 44 publications

Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats

Maternal Nicotine Exposure Exacerbates Neonatal Hyperoxia-Induced Lung Fibrosis in Rats

Effects of perinatal nicotine exposure on the development of albino rat’s alveoli with special reference to the role of the vascular endothelial growth factor

Developmental genetics of the COPD lung

Contact Info

Product

Resources

About