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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
Published on: October 19, 2013
Prenatal nicotine exposure increases connective tissue expression in foetal monkey pulmonary vessels
H S Sekhon1, B J Proskocil, J A Clark
1Division of Neuroscience, Oregon National Primate Research Center, 505 NW 185th Ave, Beaverton, OR 97006, USA. Sekhonh@ohsu.edu
The European Respiratory Journal
|June 29, 2004
Summary
Maternal smoking during pregnancy exposes fetuses to nicotine, altering pulmonary vessel structure. Nicotine affects connective tissue in fetal lungs, potentially leading to persistent pulmonary hypertension.
Area of Science:
- Obstetrics and Gynecology
- Pulmonology
- Developmental Biology
Background:
- Maternal smoking during pregnancy is linked to adverse fetal outcomes, including persistent pulmonary hypertension.
- Nicotinic acetylcholine receptors (nAChR) are present in pulmonary vasculature, suggesting a direct role for nicotine in fetal lung development.
Purpose of the Study:
- To investigate the effects of maternal nicotine exposure on fetal pulmonary vasculature structure and connective tissue expression in a rhesus monkey model.
Main Methods:
- Timed-pregnant rhesus monkeys received daily nicotine injections via osmotic mini-pumps throughout gestation.
- Fetal lung tissues were analyzed using morphometry, in situ hybridization, and immunohistochemical staining.
Main Results:
- Nicotine exposure significantly increased the thickness of airway-associated vessel walls and adventitia.
- Collagen mRNA and protein levels increased, while elastin protein levels decreased in the pulmonary vessels.
- Alpha7 nAChR and choline acetyltransferase were detected in cells of the pulmonary vessels, indicating a potential signaling pathway.
Conclusions:
- Maternal nicotine exposure alters fetal pulmonary vascular connective tissue, suggesting a mechanism for smoking-induced pulmonary hypertension.
- Nicotine's interaction with nAChR in pulmonary vessels may mediate these structural changes.

