Influence of SelS gene silence on beta-Mercaptoethanol-mediated endoplasmic reticulum stress and cell apoptosis in HepG2 cells.

Selenoprotein S (SelS), a transmembrane selenoprotein, may be related to the response of endoplasmic reticulum (ER) stress. In this report, the influence of selenite supplementation and SelS gene silence on beta-mercaptoethanol (beta-ME)-mediated ER stress and cell apoptosis in HepG2 cells were examined. The results showed that SelS protein expression was markedly increased by 10 mM beta-ME and 100 nM sodium selenite in HepG2 cells. GRP78 protein level was significantly increased after treatment with 10 mM beta-ME in HepG2 cells, which suggested that beta-ME was also an ER stress inducer. Meanwhile, beta-ME (10 mM) was found to induce cell apoptosis, which was alleviated obviously when cells were pretreated with 100 nM selenite before exposure to beta-ME. Moreover, the suppression of SelS gene by siRNA could aggravate HepG2 cell apoptosis induced by beta-ME significantly. In conclusion, these results suggested that beta-ME, also an ER stress agent, could induce cell apoptosis, and SelS may play an important role in protecting cells from apoptosis induced by ER stress in HepG2 cells. Copyright 2010 Elsevier B.V. All rights reserved.