Basal chloride currents in murine airway epithelial cells: modulation by CFTR.

Basal chloride currents in murine airway epithelial cells: modulation by CFTR.
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小鼠气道上皮细胞中的基础氯电流:CFTR 的调节。

DOI:
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发表时间:
1998
期刊:
American Journal of Physiology - Cell Physiology
影响因子:
--
通讯作者:
B. Argent
B. Argent
中科院分区:
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文献类型:
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作者:
R. Tarran;M. Gray;M. J. Evans;W. Colledge;R. Ratcliff;B. Argent

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我们从野生型和囊性纤维化(CF)空小鼠的鼻上皮分离纤毛呼吸细胞,并使用膜片钳技术研究其基础电导。未受刺激的细胞的电流钳实验表明存在的K+和Cl-电导,并在一定条件下,一个小的Na+电导。电压钳实验显示三个不同的Cl-电导。I tv-indep不依赖于时间和电压,具有线性电流-电压(I-V)图; I v-act在电位大于± 50 mV时抑制激活,给出S形I-V图; I hyp-act被超极化电位激活,具有向内整流的I-V图。电流密度的大小顺序为I hyp-act = I v-act = I tv-indep。这些电导率的Cl-与N-甲基-D-葡糖胺阳离子渗透率比值在2.8和10.3之间,不受他莫昔芬、氟芬那酯、格列本脲、DIDS和5-硝基-2-(3-苯丙氨基)苯甲酸的影响,但受Zn 2+和Gd 3+的抑制。I tv-indep和I v-act以相等的密度和频率存在于野生型和CF细胞中。然而,与野生型细胞的26%相比,仅在3%的CF细胞中检测到I hyp-act,这表明这种传导可能受到囊性纤维化跨膜传导调节因子(CFTR)的调节。
We have isolated ciliated respiratory cells from the nasal epithelium of wild-type and cystic fibrosis (CF) null mice and used the patch-clamp technique to investigate their basal conductances. Current-clamp experiments on unstimulated cells indicated the presence of K+ and Cl- conductances and, under certain conditions, a small Na+conductance. Voltage-clamp experiments revealed three distinct Cl- conductances. I tv-indep was time and voltage independent with a linear current-voltage ( I- V) plot; I v-actexhibited activation at potentials greater than ±50 mV, giving an S-shaped I- Vplot; and I hyp-act was activated by hyperpolarizing potentials and had an inwardly rectified I- Vplot. The current density sequence was I hyp-act = I v-act ≫ I tv-indep. These conductances had Cl--to- N-methyl-d-glucamine cation permeability ratios of between 2.8 and 10.3 and were unaffected by tamoxifen, flufenamate, glibenclamide, DIDS, and 5-nitro-2-(3-phenylpropylamino) benzoic acid but were inhibited by Zn2+ and Gd3+. I tv-indep and I v-act were present in wild-type and CF cells at equal density and frequency. However, I hyp-actwas detected in only 3% of CF cells compared with 26% of wild-type cells, suggesting that this conductance may be modulated by cystic fibrosis transmembrane conductance regulator (CFTR).
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