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慢性间歇性低氧大鼠颈动脉体球细胞中 p11 和 TASK1 通道的表达。

Expression of p11 and TASK1 Channels in Rat Carotid Body Glomus Cells Subjected to Chronic Intermittent Hypoxia.

机构信息

Department of Cell and Systems Physiology, School of Medicine, University of Occupational and Environmental Health, Japan.

University of Opole, Poland.

出版信息

J UOEH. 2022;44(3):249-255. doi: 10.7888/juoeh.44.249.

Abstract

Chronic intermittent hypoxia (CIH) has been used as a model to mimic nocturnal apnea, which is associated with hypertension. One of the mechanisms for hypertension in patients with nocturnal apnea is an enhancement of the plasma membrane response to acute hypoxia in carotid body glomus cells. Hypoxia is known to induce depolarization via inhibiting TWIK-related acid-sensitive K (TASK) channels, one type of leak K channels, in glomus cells. The present experiment was undertaken to immunocytochemically investigate the effects of CIH on the expression and intracellular localization of TASK1 channels and p11 that critically affect the trafficking of TASK1 to the cell surface. The expression levels of TASK1 proteins and p11 and their intracellular localization in rat carotid body glomus cells were not noticeably affected by CIH, suggesting that the enhanced membrane response to acute hypoxia is not due to an increase in surface TASK channels.

摘要

慢性间歇性低氧(CIH)已被用作模拟夜间呼吸暂停的模型,后者与高血压有关。夜间呼吸暂停患者高血压的机制之一是颈动脉体球细胞的细胞膜对急性低氧的反应增强。已知低氧通过抑制 TWIK 相关酸敏感钾(TASK)通道,即一种漏钾通道,在球细胞中诱导去极化。本实验通过免疫细胞化学方法研究了 CIH 对 TASK1 通道和 p11 的表达和细胞内定位的影响,这对 TASK1 向细胞表面的运输至关重要。CIH 对大鼠颈动脉体球细胞中 TASK1 蛋白和 p11 的表达水平及其细胞内定位没有明显影响,这表明对急性低氧的膜反应增强不是由于表面 TASK 通道的增加所致。

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