The knockdown of TASK-1 channels improved the proliferation of N2A cells.
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.
Department of Neuroscience, South-Central University for Nationalities, 182 Minyuan Road, 430074, Wuhan, China.
Xuran
X
Hao
Xiantao
X
Li
D000818:Animals; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D051379:Mice; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D024683:Potassium Channels, Tandem Pore Domain / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
D009419:Nerve Tissue Proteins; D024683:Potassium Channels, Tandem Pore Domain; D012333:RNA, Messenger; C420132:potassium channel subfamily K member 3