Kuo Tsun-Cheng, Lin-Shiau Shoei-Yn
Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan.
Neurochem Res. 2004 Jul;29(7):1453-9. doi: 10.1023/b:nere.0000026411.84915.55.
Ca2+-activated K+ channels were studied in C6-glioma cells in an attempt to correlate changes in expression with cell proliferation and differentiation. In this study, we treated C6-glioma cells with thapsigargin for 48 h. Cell proliferation was markedly inhibited, and cell morphology changed from round to a spindle differentiated shape. Furthermore, intracellular calcium concentration was initially increased during acute treatment with thapsigargin. The internal [Ca2+]i pool was eventually depleted after a 48-h thapsigargin treatment. We have characterized Ca2+-activated K+ currents in less differentiated C6 cells. After differentiation of C6 cells induced by thapsigargin, Ca2+-activated K+ currents were selectively suppressed. These data lend further support to the notion that the expression of Ca2+-activated K+ channels is intimately associated with the proliferation of C6-glioma cells, and the suppression of Ca2+-activated K+ channels coincides with the inhibition of proliferation and subsequent induction of cell differentiation.
为了将表达变化与细胞增殖和分化联系起来,对C6胶质瘤细胞中的钙激活钾通道进行了研究。在本研究中,我们用毒胡萝卜素处理C6胶质瘤细胞48小时。细胞增殖受到明显抑制,细胞形态从圆形变为纺锤形的分化形态。此外,在用毒胡萝卜素急性处理期间,细胞内钙浓度最初会升高。经过48小时的毒胡萝卜素处理后,细胞内[Ca2+]i池最终耗尽。我们已经对分化程度较低的C6细胞中的钙激活钾电流进行了表征。在用毒胡萝卜素诱导C6细胞分化后,钙激活钾电流被选择性抑制。这些数据进一步支持了以下观点:钙激活钾通道的表达与C6胶质瘤细胞的增殖密切相关,钙激活钾通道的抑制与增殖抑制以及随后的细胞分化诱导相吻合。