Journal
PLACENTA
Volume 71, Issue -, Pages 16-23Publisher
W B SAUNDERS CO LTD
DOI: 10.1016/j.placenta.2018.09.008
Keywords
Immunostaining; Infant; Nicotine; Protein; Tobacco smoke
Funding
- Preeclampsia Research Laboratories (PEARLS)
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Introduction: Cigarette smoking (CS) and preeclampsia (PE), regulate the expression of nicotinic acetylcholine receptor (nAChR) subunits in the placenta, yet no data exist at the histological level. Methods: Using immunohistochemistry of formalin fixed and paraffin embedded placental tissue, this study quantified the expression of nine nAChR subunits (alpha 2, alpha 3, alpha 4, alpha 5, alpha 7, alpha 9, beta 1, beta 2, delta) and compared the expression amongst four groups of non-smoker non-PE (controls, n = 8), smokers (n = 8), PE (n = 8), and those who were smokers with PE (smoke+ PE, n = 4). Quantification was of the percentage of villi with positive cells stained (% villi with + ve), percentage of positive stained cells per villous (% + ve cells/villous), percentage of positive cells in the decidua (%+ ve Decidua), and intensity of staining in the outer villous trophoblast layer. Results: Changes were restricted to the villi (as opposed to the decidua), and were specific to the a9 (smoke + PE), beta 1 (smokers), and beta 2 (PE) subunits when compared to controls. CS seemed to have a protective effect for the beta 2 subunit and an additive effect for the a9 and beta 1 subunits within the villous core/stroma cells and not the trophoblast layer. Discussion: These findings support that both CS and PE affect nAChRs in the placenta, but that this is restricted to the villi.
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