Fraser Scott P, Diss James K J, Lloyd Louise J, Pani Filippo, Chioni Athina-Myrto, George Andrew J T, Djamgoz Mustafa B A
Department of Biological Sciences, Sir Alexander Fleming Building, Imperial College London, South Kensington Campus, London SW7 2AZ, UK.
FEBS Lett. 2004 Jul 2;569(1-3):191-4. doi: 10.1016/j.febslet.2004.05.063.
Whole-cell patch-clamp recordings showed that a sub-population (10%) of Jurkat cells, a model of human T-cells, expressed a functional voltage-gated sodium channel, which was tetrodotoxin (TTX)-resistant. Expression of voltage-gated sodium channel protein was confirmed by western blots. Semi-quantitative PCR analysis revealed that mRNAs for the alpha-subunits of multiple voltage-gated sodium channel subtypes were present but indicated that Na(v)1.5 was the predominant subtype, consistent with the TTX-resistant nature of the recorded currents. Importantly, 10 microM TTX reduced the number of Jurkat cells invading a Matrigel basement membrane by 93.0+/-5.5%. Since similar sodium channels have also been detected in normal human T-lymphocytes, it is concluded that the activity of voltage-gated sodium channels could represent a novel mechanism potentiating the invasive capacity of these cells.
全细胞膜片钳记录显示，人类T细胞模型Jurkat细胞的一个亚群（10%）表达了一种功能性电压门控钠通道，该通道对河豚毒素（TTX）具有抗性。通过蛋白质免疫印迹法证实了电压门控钠通道蛋白的表达。半定量PCR分析表明，多种电压门控钠通道亚型的α亚基的mRNA均存在，但显示Na(v)1.5是主要亚型，这与记录电流对TTX的抗性特性一致。重要的是，10微摩尔/升的TTX使侵袭基质胶基底膜的Jurkat细胞数量减少了93.0±5.5%。由于在正常人T淋巴细胞中也检测到了类似的钠通道，因此得出结论，电压门控钠通道的活性可能代表了一种增强这些细胞侵袭能力的新机制。
