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首页> 外文期刊>International Journal of Molecular Sciences >Lead Poisoning Disturbs Oligodendrocytes Differentiation Involved in Decreased Expression of NCX3 Inducing Intracellular Calcium Overload
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Lead Poisoning Disturbs Oligodendrocytes Differentiation Involved in Decreased Expression of NCX3 Inducing Intracellular Calcium Overload

机译：铅中毒干扰少突胶质细胞分化，参与诱导NCX3表达降低诱导细胞内钙超载

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摘要

Lead (Pb) poisoning has always been a serious health concern, as it permanently damages the central nervous system. Chronic Pb accumulation in the human body disturbs oligodendrocytes (OLs) differentiation, resulting in dysmyelination, but the molecular mechanism remains unknown. In this study, Pb at 1 μM inhibits OLs precursor cells (OPCs) differentiation via decreasing the expression of Olig 2, CNPase proteins in vitro. Moreover, Pb treatment inhibits the sodium/calcium exchanger 3 (NCX3) mRNA expression, one of the major means of calcium (Ca2+) extrusion at the plasma membrane during OPCs differentiation. Also addition of KB-R7943, NCX3 inhibitor, to simulate Pb toxicity, resulted in decreased myelin basic protein (MBP) expression and cell branching. Ca2+ response trace with Pb and KB-R7943 treatment did not drop down in the same recovery time as the control, which elevated intracellular Ca2+ concentration reducing MBP expression. In contrast, over-expression of NCX3 in Pb exposed OPCs displayed significant increase MBP fluorescence signal in positive regions and CNPase expression, which recovered OPCs differentiation to counterbalance Pb toxicity. In conclusion, Pb exposure disturbs OLs differentiation via affecting the function of NCX3 by inducing intracellular calcium overload.
机译：铅（Pb）中毒一直是严重的健康问题，因为它会永久损害中枢神经系统。人体中长期积累的Pb会干扰少突胶质细胞（OLs）的分化，导致髓鞘脱髓鞘，但分子机制尚不清楚。在这项研究中，1μM的Pb通过降低体外Olig 2，CNPase蛋白的表达来抑制OLs前体细胞（OPC）的分化。此外，铅处理抑​​制了钠/钙交换子3（NCX3）mRNA的表达，这是OPC分化过程中质膜上钙（Ca 2 + ）挤出的主要手段之一。还添加了NCX3抑制剂KB-R7943，以模拟Pb毒性，导致髓鞘碱性蛋白（MBP）的表达和细胞分支减少。铅和KB-R7943处理的Ca 2 + 反应曲线在与对照组相同的恢复时间内没有下降，这增加了细胞内Ca 2 + 的浓度，降低了MBP的表达。相反，暴露于Pb的OPC中NCX3的过表达在阳性区域和CNPase表达中显示出MBP荧光信号显着增加，从而恢复了OPC的分化，从而抵消了Pb的毒性。总之，Pb暴露通过诱导细胞内钙超载影响NCX3的功能，从而干扰OLs的分化。

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