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Characterization of CFTR expression and chloride channel activity in human endothelia.

机译:人内皮中CFTR表达和氯离子通道活性的表征。

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摘要

The cystic fibrosis transmembrane conductance regulator (CFTR) functions as a low-conductance, cAMP-regulated chloride (Cl-) channel in a variety of cell types, such as exocrine epithelial cells. Our results demonstrate that human primary endothelial cells isolated from umbilical vein (HUVEC) and lung microvasculature (HLMVEC) also express CFTR as determined via RT-PCR and immunohistochemical and immunoprecipitation analyses. Moreover, Cl- efflux and whole cell patch-clamp analyses reveal that HUVEC (n = 6 samples, P < 0.05) and HLMVEC (n = 5 samples, P < 0.05) display cyclic nucleotide-stimulated Cl- transport that is inhibited by the CFTR selective Cl- channel blocker glibenclamide but not by the blocker DIDS, indicative of CFTR Cl- channel activity. Taken together, these findings demonstrate that human endothelial cells derived from multiple organ systems express CFTR and that CFTR functions as a cyclic nucleotide-regulated Cl- channel in human endothelia.
机译:囊性纤维化跨膜电导调节器(CFTR)在多种细胞类型(例如外分泌上皮细胞)中充当低电导,cAMP调节的氯离子(Cl-)通道。我们的结果表明,通过RT-PCR以及免疫组织化学和免疫沉淀分析确定,从脐静脉(HUVEC)和肺微脉管系统(HLMVEC)分离出的人原代内皮细胞也表达CFTR。此外,Cl-流出和全细胞膜片钳分析显示,HUVEC(n = 6个样品,P <0.05)和HLMVEC(n = 5个样品,P <0.05)显示出环状核苷酸刺激的Cl-转运,该转运受到抑制。 CFTR选择性C1通道阻滞剂格列本脲但不被DIDS阻滞剂所指示,表明CFTR C1通道的活性。综上所述,这些发现证明源自多个器官系统的人内皮细胞表达CFTR,并且CFTR在人内皮中充当环核苷酸调节的Cl-通道。

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