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首页> 外文期刊>American Journal of Physiology >TMEM16A channels generate Ca2+-activated Cl- currents in cerebral artery smooth muscle cells.
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TMEM16A channels generate Ca2+-activated Cl- currents in cerebral artery smooth muscle cells.

机译：TMEM16A通道在脑动脉平滑肌细胞中产生Ca2 +激活的Cl-电流。

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摘要

Transmembrane protein (TMEM)16A channels are recently discovered membrane proteins that display electrophysiological properties similar to classic Ca(2+)-activated Cl(-) (Cl(Ca)) channels in native cells. The molecular identity of proteins that generate Cl(Ca) currents in smooth muscle cells (SMCs) of resistance-size arteries is unclear. Similarly, whether cerebral artery SMCs generate Cl(Ca) currents is controversial. Here, using molecular biology and patch-clamp electrophysiology, we examined TMEM16A channel expression and characterized Cl(-) currents in arterial SMCs of resistance-size rat cerebral arteries. RT-PCR amplified transcripts for TMEM16A but not TMEM16B-TMEM16H, TMEM16J, or TMEM16K family members in isolated pure cerebral artery SMCs. Western blot analysis using an antibody that recognized recombinant (r)TMEM16A channels detected TMEM16A protein in cerebral artery lysates. Arterial surface biotinylation and immunofluorescence indicated that TMEM16A channels are located primarily within the arterial SMC plasma membrane. Whole cell Cl(Ca) currents in arterial SMCs displayed properties similar to those generated by rTMEM16A channels, including Ca(2+) dependence, current-voltage relationship linearization by an elevation in intracellular Ca(2+) concentration, a Nerstian shift in reversal potential induced by reducing the extracellular Cl(-) concentration, and a negative reversal potential shift when substituting extracellular I(-) for Cl(-). A pore-targeting TMEM16A antibody similarly inhibited both arterial SMC Cl(Ca) and rTMEM16A currents. TMEM16A knockdown using small interfering RNA also inhibited arterial SMC Cl(Ca) currents. In summary, these data indicate that TMEM16A channels are expressed, insert into the plasma membrane, and generate Cl(Ca) currents in cerebral artery SMCs.
机译：跨膜蛋白（TMEM）16A通道是最近发现的膜蛋白，其显示的电生理特性类似于天然细胞中经典的Ca（2+）激活的Cl（-）（Cl（Ca））通道。尚不清楚在阻力大小动脉的平滑肌细胞（SMC）中产生Cl（Ca）电流的蛋白质的分子身份。同样，脑动脉SMC是否产生Cl（Ca）电流也存在争议。在这里，我们使用分子生物学和膜片钳电生理学，我们检查了TMEM16A通道的表达，并表征了具有抗药性的大鼠脑动脉的SMC中的Cl（-）电流。 RT-PCR扩增了分离的纯脑动脉SMC中TMEM16A而不是TMEM16B-TMEM16H，TMEM16J或TMEM16K家族成员的转录本。使用识别重组（r）TMEM16A通道的抗体进行的蛋白质印迹分析在脑动脉裂解液中检测到TMEM16A蛋白。动脉表面生物素化和免疫荧光表明TMEM16A通道主要位于动脉SMC质膜内。动脉SMC中的全细胞Cl（Ca）电流显示的性质类似于rTMEM16A通道生成的性质，包括Ca（2+）依赖性，通过细胞内Ca（2+）浓度升高的电流-电压关系线性化，反向的Nerstian移位降低细胞外Cl（-）浓度诱导的电势，当用细胞外I（-）代替Cl（-）时产生负的反向电势偏移。靶向孔的TMEM16A抗体同样抑制动脉SMC Cl（Ca）和rTMEM16A电流。使用小干扰RNA的TMEM16A敲低也抑制了动脉SMC Cl（Ca）电流。总之，这些数据表明，TMEM16A通道已表达，插入质膜并在脑动脉SMC中产生Cl（Ca）电流。

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