Antioxidative role of selenoprotein W in oxidant-induced mouse embryonic neuronal cell death
Antioxidative role of selenoprotein W in oxidant-induced mouse embryonic neuronal cell death
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DOI：
10.1007/s10059-009-0074-3
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发表时间：
2009-05-01
影响因子：
3.8
通讯作者：
Kim, Ick Young
中科院分区：
文献类型：
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作者：
Chung, Youn Wook;Jeong, Daewon;Kim, Ick Young
有报道称，硒蛋白W(SelW)在发育中的大鼠中枢神经系统中高表达，并且一直维持到出生后早期。我们在这里发现出生后第8天和第20天的小鼠大脑中SelW蛋白比胚胎第15天显著增加。这伴随着SOD1和SOD2的表达增加。用小干扰RNA(SiRNAs)抑制胚脑皮质来源的原代培养细胞SelW的表达后，转染SelW siRNA的神经细胞对H_2O_2诱导的氧化应激比对照细胞更敏感。TUNEL检测显示，在siRNA转染组细胞中，H_2O_2诱导的细胞死亡的频率高于对照组。综上所述，我们的研究结果表明，SelW在神经元发育过程中保护神经元免受氧化应激的影响发挥着重要作用。
It has been reported that selenoprotein W (SelW) mRNA is highly expressed in the developing central nerve system of rats, and its expression is maintained until the early postnatal stage. We here found that SelW protein significantly increased in mouse brains of postnatal day 8 and 20 relative to embryonic day 15. This was accompanied by increased expression of SOD1 and SOD2. When the expression of SelW in primary cultured cells derived from embryonic cerebral cortex was knocked down with small interfering RNAs (siRNAs), SelW siRNA-transfected neuronal cells were more sensitive to the oxidative stress induced by treatment of H2O2 than control cells. TUNEL assays revealed that H2O2-induced apoptotic cell death occurred at a higher frequency in the siRNA-transfected cells than in the control cells. Taken together, our findings suggest that SelW plays an important role in protection of neurons from oxidative stress during neuronal development.