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Int. J. Mol. Sci. 2014, 15(11), 21331-21347;

Se-Methylselenocysteine Inhibits Apoptosis Induced by Clusterin Knockdown in Neuroblastoma N2a and SH-SY5Y Cell Lines

2,* , 4
Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China
Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences, Shenzhen University, Shenzhen 518060, China
University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing 100049, China
Microorganism Examination Division, Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Received: 18 September 2014 / Revised: 7 November 2014 / Accepted: 7 November 2014 / Published: 18 November 2014
(This article belongs to the Special Issue RNA Interference)
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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. View Full-Text
Keywords: clusterin (Clu); Se-methylselenocysteine (MSC); cell apoptosis; RNA interference (RNAi); gene knockdown clusterin (Clu); Se-methylselenocysteine (MSC); cell apoptosis; RNA interference (RNAi); gene knockdown

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Wang, C.; Zeng, Z.; Liu, Q.; Zhang, R.; Ni, J. Se-Methylselenocysteine Inhibits Apoptosis Induced by Clusterin Knockdown in Neuroblastoma N2a and SH-SY5Y Cell Lines. Int. J. Mol. Sci. 2014, 15, 21331-21347.

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