Se-Methylselenocysteine Inhibits Apoptosis Induced by Clusterin Knockdown in Neuroblastoma N2a and SH-SY5Y Cell Lines
Se-Methylselenocysteine Inhibits Apoptosis Induced by Clusterin Knockdown in Neuroblastoma N2a and SH-SY5Y Cell Lines
复制标题
Se-甲基硒代半胱氨酸抑制神经母细胞瘤 N2a 和 SH-SY5Y 细胞系中簇蛋白敲低诱导的细胞凋亡
DOI:
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发表时间:
2014
影响因子:
5.6
通讯作者:
Jiazuan Ni
中科院分区:
文献类型:
--
作者:
Chao Wang;Z. Zeng;Qiong Liu;Renli Zhang;Jiazuan Ni
Apoptosis, as a programmed cell death process, is essential for the maintenance of tissue function in organisms. Alteration of this process is linked to many diseases. Over-expression of clusterin (Clu) can antagonize apoptosis in various cells. Selenium (Se) is an essential trace element for human health. Its biological function is also associated with cell apoptosis. To explore the function of Clu and the impact of Se in the process of apoptosis, several short-hairpin RNAs (shRNA) were designed for the construction of two sets of recombinant plasmids: one set for plasmid-transfection of mouse neuroblastoma N2a cells (N2a cells); and the other set for lentiviral infection of human neuroblastoma SH-SY5Y cells (SH-SY5Y cells). These shRNAs specifically and efficiently interfered with the intracellular expression of Clu at both the mRNA and protein levels. The Clu-knockdown cells showed apoptosis-related features, including down-regulation of antioxidative capacity and the Bcl-2/Bax ratio and up-regulation of caspase-8 activity. Se-methylselenocysteine (MSC) at an optimum concentration of 1 μM could reverse the alteration in antioxidative capacity, Bcl2/Bax ratio and caspase-8 activity caused by Clu-knockdown, thus inhibiting apoptosis and maintaining cell viability. The results hereby imply the potentiality of Clu and Se in neuroprotection.
DOI:
10.1152/ajpregu.2000.278.3.r640
发表时间:
2000
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
作者:
Yoo,KH;Thornhill,BA;Chevalier,RL
通讯作者:
Chevalier,RL