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脂多糖可迅速激活大鼠脑动脉平滑肌细胞内膜表面的钾离子通道。

Lipopolysaccharide rapidly activates K+ channels at the intracellular membrane face of rat cerebral artery smooth muscle cells.

作者信息

Hoang L M, Chen C, Mathers D A

机构信息

Department of Physiology, Faculty of Medicine, University of British Columbia, Vancouver, Canada.

出版信息

Neurosci Lett. 1997 Aug 1;231(1):25-8. doi: 10.1016/s0304-3940(97)00519-3.

Abstract

Lipopolysaccharide (LPS) may accumulate inside mammalian cells through endocytotic uptake or during the replication in invasive bacterial strains. However, the effects of intracellular LPS on cell function remain unknown. This study therefore examined the action of intracellularly applied E. coli LPS on large-conductance, Ca2+-dependent K+ channels (BK channels) in the membrane of rat cerebrovascular smooth muscle cells (CVSMCs). LPS (10-100 microg/ml) rapidly increased the open probability of BK channels when applied to the cytoplasmic face of CVSMC membrane patches. This response was reversible, dose-dependent and reflected an enhanced rate of channel opening in the presence of LPS. These results show for the first time that LPS can alter the gating behavior of ionic channels when applied to the cytoplasmic face of a eukaryotic cell membrane.

摘要

脂多糖(LPS)可通过内吞摄取作用在哺乳动物细胞内蓄积,或在侵袭性细菌菌株的复制过程中蓄积。然而,细胞内LPS对细胞功能的影响尚不清楚。因此,本研究检测了细胞内应用的大肠杆菌LPS对大鼠脑血管平滑肌细胞(CVSMC)膜上大电导、Ca2+依赖性钾通道(BK通道)的作用。当将LPS(10 - 100微克/毫升)应用于CVSMC膜片的胞质面时,可迅速增加BK通道的开放概率。这种反应是可逆的、剂量依赖性的,反映了在LPS存在下通道开放速率的提高。这些结果首次表明,当LPS应用于真核细胞膜的胞质面时,可改变离子通道的门控行为。

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