Effect of e-cigarette vapour extraction on vasoactive gene expression in human pulmonary artery smooth muscle and endothelial cells.

Abstract

Introduction: Pulmonary Hypertension (PH) is a common and serious complication of COPD. We previously demonstrated that Cigarette Smoke Extracts (CSE) induced imbalanced vasoactive gene expression in human Pulmonary Artery Smooth Muscle Cells (hPASMCs) and Pulmonary artery endothelial cells (hPAECs). Although increasing evidence shows that electronic cigarette (e-cigarette) containing nicotine is associated with increased risk of cardiovascular disease, the effect of e-cigarette vapour extraction (ECVE) on vasoactive gene expression in hPASMCs and hPAECs is unknown. We hypothesize that ECVE may have similar effects as CSE on the induction of an imbalance between excessive vasoconstrictors and deficient vasodilators, which then contributes to aberrant hPASMC proliferation in COPD-associated PH and can be a target for therapeutic intervention. Methods: ECVE was prepared the same way as CSE from 6 ml e-cigarette liquid (0.24 mg/ml nicotine, total nicotine the same as two cigarettes used for CSE). Confluent hPASMCs and hPAECs were treated with different concentrations of ECVE. Western blotting and real-time RT-PCR were used to assess protein and mRNA expression of Prostacyclin Synthase (PGIS), and Cyclooxygenase-2 (COX-2), Endothelial Nitric Oxide Synthase (eNOS), Thromboxane A Synthase (TXAS), Endothelin 1(ET-1), respectively. Results: ECVE reduced the protein and mRNA expression of eNOS and PGIS and upregulated COX-2 and TXAS level in a concentration-dependent manner. Interestingly, ECVE did not have any effect on ET-1. Conclusion: Our findings suggest that ECVE may have similar effects on imbalanced vasoactive gene expression as CSE.