Critical role of L-type voltage-dependent Ca2+ channels in neural progenitor cell proliferation induced by hypoxia
Critical role of L-type voltage-dependent Ca2+ channels in neural progenitor cell proliferation induced by hypoxia
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DOI：
10.1016/j.neulet.2010.05.007
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发表时间：
2010-07-12
影响因子：
2.5
通讯作者：
Wang, Xiaomin
中科院分区：
文献类型：
--
作者：
Guo, Zixuan;Shi, Fang;Wang, Xiaomin
体外和体内缺氧均可促进神经祖细胞的增殖，但其机制尚不清楚。钙离子对祖细胞的增殖有重要作用。在这项研究中，我们报道了Ca2+通过l型电压依赖性Ca2+通道内流介导的缺氧促进了从胚胎14.5天的大鼠中脑分离的神经祖细胞的增殖。与正常缺氧（20% O-2, 72 h）相比，生理缺氧（3% O-2, 72 h）培养的神经祖细胞细胞数量显著增加。当细胞暴露于缺氧时，也观察到细胞内Ca2+浓度增加。此外，去除细胞外Ca2+或给予尼卡地平（一种已知阻断l型Ca2+通道的药物），可抑制缺氧诱导的细胞内Ca2+和细胞数量的增加。这些结果表明，缺氧通过增加Ca2+内流促进神经祖细胞的增殖，这可能是l型电压依赖性Ca2+通道功能上调的结果。2010爱思唯尔爱尔兰有限公司版权所有。
Hypoxia can promote proliferation of neural progenitor cells in vitro and in vivo, however, the mechanisms underlying this phenomenon remain largely unknown. Calcium ions are important for the proliferation of progenitor cells. In this study, we reported that Ca2+ influx through L-type voltage-dependent Ca2+ channels mediated hypoxia-promoted proliferation of neural progenitor cells isolated from embryonic day 14.5 rat mesencephalon. Cell number was greatly increased in the cultured neural progenitor cells exposed to physiological hypoxia (3% O-2, 72 h) compared with normoxia exposure (20% O-2, 72 h). Increased intracellular Ca2+ concentration was also observed when the cells were exposed to hypoxia. Moreover, removal of extracellular Ca2+ or administration of nicardipine, an agent known to block L-type Ca2+ channels, resulted in suppression of the hypoxia-induced increase in intracellular Ca2+ and cell numbers. These results suggest that hypoxia promoted the proliferation of neural progenitor cells by increasing Ca2+ influx, which was likely a result of upregulation of L-type voltage-dependent Ca2+ channel function. (c) 2010 Elsevier Ireland Ltd. All rights reserved.