國家衛生研究院 NHRI:Item 3990099045/2543
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    題名: Inhibition of alpha 7-nicotinic acetylcholine receptor expression by arsenite in the vascular endothelial cells
    作者: Hsu, SH;Tsou, TC;Chiu, SJ;Chao, JI
    貢獻者: Division of Environmental Health and Occupational Medicine
    摘要: The alpha 7-nicotinic acetylcholine receptor (alpha 7-nAChR), expressed in the neuronal and non-neuronal cells, has been shown to regulate cell proliferation. However, the expression and function of the alpha 7-nAChR in the proliferation of the vascular endothelial cells remain unclear. In this study, we investigated the expression of the alpha 7-nAChR in the arsenite-exposed vascular endothelial cells. The vascular endothelial cells SVEC4-10 and porcine aorta endothelial cells (PAEC) expressed the a7-nAChR proteins. Moreover, the location of the alpha 7-nAChR proteins on cell membrane of the vascular endothelial cells was identified by the alpha 7-nAChR binding to a tetramethylrhodamine-labeled a-bungarotoxin (alpha-BTX). Arsenite (20 mu LM, 24 h) significantly induced the cytotoxicity, cell growth inhibition, and apoptosis in the vascular endothelial cells. The level of alpha 7-nAChR proteins was concentration dependently decreased in the arsenite-treated endothelial cells. Furthermore, a specific alpha 7-nAChR antagonist, alpha-BTX, inhibited the cell viability in the vascular endothelial cells. Nevertheless, alpha-BTX, and a alpha 7-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 alpha 7-nAChR protein expression and cause the cell injury in the vascular endothelial cells. (c) 2005 Elsevier Ireland Ltd. All rights reserved.
    關鍵詞: Toxicology
    日期: 2005-10-15
    關聯: Toxicology Letters. 2005 Oct;159(1):47-59.
    Link to: http://dx.doi.org/10.1016/j.toxlet.2005.04.012
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0378-4274&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000232676700006
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=24944438168
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