The Knockdown of TASK-1 Channels Improved the Proliferation of N2A Cells

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• 作者：Xuran Hao (1)
  Xiantao Li (1)
  
  1. Department of Neuroscience ; South-Central University for Nationalities ; 182 Minyuan Road ; 430074 ; Wuhan ; China
  
• 关键词：TASK ; 1 channels ; siRNA ; Cell proliferation ; N2A cells
• 刊名：Journal of Molecular Neuroscience
• 出版年：2015
• 出版时间：February 2015
• 年：2015
• 卷：55
• 期：2
• 页码：314-317
• 全文大小：205 KB
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• 刊物主题：Neurosciences; Neurochemistry; Cell Biology; Proteomics; Neurology;
• 出版者：Springer US
• ISSN：1559-1166

文摘

Previous studies indicated that K+ channels, such as voltage-gated Kv channels, were involved in the apoptosis and proliferation of neurons. In the experiments here, the small interfering RNAs (siRNAs) targeted against TASK-1, an acid-sensitive member of two-pore domain K+ (K2P) channel family, were transfected into mouse neuroblastoma N2A cells. This treatment induced a reduction of messenger RNA (mRNA) level of TASK-1 by 61 %. As a negative control, however, the transfection of scrambled siRNAs (scRNA) did not significantly affect the expression of TASK-1 in N2A cells. Furthermore, exposure to TASK-1-specific siRNAs (siTASK-1) for 48 h also substantially increased the proliferation rates of N2A cells by 25.8 %, but no effect was observed in scRNA-treated cells. These data implied that TASK-1 channels may participate in the regulation of neuronal proliferation.