Dichotomous effects of aryl hydrocarbon receptor (AHR) activation on human fetoplacental endothelial cell function.

ABSTRACT:

Introduction

Maternal cigarette smoking is associated with elevated fetoplacental vascular resistance and fetal growth restriction (FGR). While studies have demonstrated varying effects of nicotine on blood flow, the role of polycyclic aromatic hydrocarbons (PAHs), abundant toxins in cigarette smoke that cross the placenta, has not been elucidated. We hypothesized that exposure of human fetoplacental endothelial cells (ECs) to the PAH benzo[a]yrene (BaP) would result in up-regulation of cyclooxygenase-2 (PTGS2) and preferential production of vasoconstrictive prostanoids via activation of the aryl hydrocarbon receptor (AHR) pathway.

Methods

ECs were isolated, cultured, and treated with vehicle or BaP. ECs were subjected to real-time PCR, western blotting, enzyme immunoassays,

SUBMITTER: Palatnik A 

PROVIDER: S-EPMC4964606 | biostudies-literature | 2016 Aug

REPOSITORIES: biostudies-literature