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  • Title: Inhibition of alpha7-nicotinic acetylcholine receptor expression by arsenite in the vascular endothelial cells.
    Author: Hsu SH, Tsou TC, Chiu SJ, Chao JI.
    Journal: Toxicol Lett; 2005 Oct 15; 159(1):47-59. PubMed ID: 15961264.
    Abstract:
    The alpha7-nicotinic acetylcholine receptor (alpha7-nAChR), expressed in the neuronal and non-neuronal cells, has been shown to regulate cell proliferation. However, the expression and function of the alpha7-nAChR in the proliferation of the vascular endothelial cells remain unclear. In this study, we investigated the expression of the alpha7-nAChR in the arsenite-exposed vascular endothelial cells. The vascular endothelial cells SVEC4-10 and porcine aorta endothelial cells (PAEC) expressed the alpha7-nAChR proteins. Moreover, the location of the alpha7-nAChR proteins on cell membrane of the vascular endothelial cells was identified by the alpha7-nAChR binding to a tetramethylrhodamine-labeled alpha-bungarotoxin (alpha-BTX). Arsenite (20 microM, 24 h) significantly induced the cytotoxicity, cell growth inhibition, and apoptosis in the vascular endothelial cells. The level of alpha7-nAChR proteins was concentration dependently decreased in the arsenite-treated endothelial cells. Furthermore, a specific alpha7-nAChR antagonist, alpha-BTX, inhibited the cell viability in the vascular endothelial cells. Nevertheless, alpha-BTX, and a alpha7-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 alpha7-nAChR protein expression and cause the cell injury in the vascular endothelial cells.
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