Inhibition of α7-nicotinic acetylcholine receptor expression by arsenite in the vascular endothelial cells

The α7-nicotinic acetylcholine receptor (α7-nAChR), expressed in the neuronal and non-neuronal cells, has been shown to regulate cell proliferation. However, the expression and function of the α7-nAChR in the proliferation of the vascular endothelial cells remain unclear. In this study, we investigated the expression of the α7-nAChR in the arsenite-exposed vascular endothelial cells. The vascular endothelial cells SVEC4-10 and porcine aorta endothelial cells (PAEC) expressed the α7-nAChR proteins. Moreover, the location of the α7-nAChR proteins on cell membrane of the vascular endothelial cells was identified by the α7-nAChR binding to a tetramethylrhodamine-labeled α-bungarotoxin (α-BTX). Arsenite (20 μM, 24 h) significantly induced the cytotoxicity, cell growth inhibition, and apoptosis in the vascular endothelial cells. The level of α7-nAChR proteins was concentration dependently decreased in the arsenite-treated endothelial cells. Furthermore, a specific α7-nAChR antagonist, α-BTX, inhibited the cell viability in the vascular endothelial cells. Nevertheless, α-BTX, and a α7-nAChR agonist, nicotine, did not significantly alter the cytotoxicity in the arsenite-treated endothelial cells. In addition, arsenite decreased the level of endothelial nitric oxide synthase proteins but did not alter choline acetyltransferase proteins in the SVEC4-10 endothelial cells. Together, our results indicate that arsenite can inhibit the α7-nAChR protein expression and cause the cell injury in the vascular endothelial cells.