Abstract
IntroductionCigarette 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. MethodsUsing immunohistochemistry of formalin fixed and paraffin embedded placental tissue, this study quantified the expression of nine nAChR subunits (α2, α3, α4, α5, α7, α9, β1, β2, δ) 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. ResultsChanges were restricted to the villi (as opposed to the decidua), and were specific to the α9 (smoke + PE), β1 (smokers), and β2 (PE) subunits when compared to controls. CS seemed to have a protective effect for the β2 subunit and an additive effect for the α9 and β1 subunits within the villous core/stroma cells and not the trophoblast layer. DiscussionThese findings support that both CS and PE affect nAChRs in the placenta, but that this is restricted to the villi.
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