Du Shaoqing, Liu Hongmei, Huang Kaixun
Hubei Key Laboratory of Bioinorganic Chemistry & Materia Medica, School of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan 430074, People's Republic of China.
Biochim Biophys Acta. 2010 May;1800(5):511-7. doi: 10.1016/j.bbagen.2010.01.005. Epub 2010 Jan 28.
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.
硒蛋白S（SelS）是一种跨膜硒蛋白，可能与内质网（ER）应激反应有关。在本报告中，研究了亚硒酸盐补充和SelS基因沉默对β-巯基乙醇（β-ME）介导的HepG2细胞内质网应激和细胞凋亡的影响。结果显示，10 mM β-ME和100 nM亚硒酸钠可使HepG2细胞中SelS蛋白表达显著增加。10 mM β-ME处理后，HepG2细胞中GRP78蛋白水平显著升高，这表明β-ME也是一种内质网应激诱导剂。同时，发现β-ME（10 mM）可诱导细胞凋亡，在暴露于β-ME之前用100 nM亚硒酸盐预处理细胞可明显减轻细胞凋亡。此外，siRNA抑制SelS基因可显著加重β-ME诱导的HepG2细胞凋亡。总之，这些结果表明，β-ME作为一种内质网应激剂可诱导细胞凋亡，SelS可能在保护HepG2细胞免受内质网应激诱导的凋亡中发挥重要作用。
