Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions
Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions
复制标题
等渗或低渗条件下大鼠腮腺腺泡细胞中 α1 肾上腺素受体诱导的 AQP5 运输激活的机制
DOI：
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发表时间：
2016
影响因子：
5.6
通讯作者：
Y. Ishikawa
中科院分区：
文献类型：
--
作者：
Aneta M. Bragiel;Di Wang;Tomasz D Pieczonka;M. Shono;Y. Ishikawa
在唾液腺中，水通道蛋白5（AQP 5）向顶端质膜（APM）的细胞运输缺陷与唾液分泌的丧失有关。为探讨α1肾上腺素能受体（AR）诱导AQP 5转运的机制，采用免疫共聚焦显微镜和Western blot分析方法，研究了不同渗透压下苯肾上腺素刺激的腮腺组织中AQP 5的定位。苯肾上腺素诱导的AQP 5向APM和侧质膜（LPM）的运输是通过α1A-AR亚型介导的，而不是通过α1B-和α1D-AR亚型介导的。ODQ和KT 5823分别是一氧化氮（NO）刺激的鸟苷酸环化酶（GC）和蛋白激酶（PK）G的抑制剂，可抑制苯肾上腺素诱导的AQP 5转运，表明NO/可溶性（c）GC/PKG信号通路参与了AQP 5转运。在等渗条件下，La 3+可抑制苯肾上腺素诱导的细胞外转运，提示钙库操纵的钙通道参与了这一过程。在低渗条件下，苯肾上腺素诱导的AQP 5向APM的运输高于等渗条件下。在非刺激条件下，低渗诱导的运输AQP 5的APM抑制钌红和镧3+，表明参与细胞外Ca 2+的进入。因此，α1A-AR激活诱导AQP 5通过Ca 2 +/环磷酸鸟苷（cGMP）/PKG信号通路运输到APM和LPM，这与钙库操作的Ca 2+内流有关。
Defective cellular trafficking of aquaporin-5 (AQP5) to the apical plasma membrane (APM) in salivary glands is associated with the loss of salivary fluid secretion. To examine mechanisms of α1-adrenoceptor (AR)-induced trafficking of AQP5, immunoconfocal microscopy and Western blot analysis were used to analyze AQP5 localization in parotid tissues stimulated with phenylephrine under different osmolality. Phenylephrine-induced trafficking of AQP5 to the APM and lateral plasma membrane (LPM) was mediated via the α1A-AR subtype, but not the α1B- and α1D-AR subtypes. Phenylephrine-induced trafficking of AQP5 was inhibited by ODQ and KT5823, inhibitors of nitric oxide (NO)-stimulated guanylcyclase (GC) and protein kinase (PK) G, respectively, indicating the involvement of the NO/ soluble (c) GC/PKG signaling pathway. Under isotonic conditions, phenylephrine-induced trafficking was inhibited by La3+, implying the participation of store-operated Ca2+ channel. Under hypotonic conditions, phenylephrine-induced trafficking of AQP5 to the APM was higher than that under isotonic conditions. Under non-stimulated conditions, hypotonicity-induced trafficking of AQP5 to the APM was inhibited by ruthenium red and La3+, suggesting the involvement of extracellular Ca2+ entry. Thus, α1A-AR activation induced the trafficking of AQP5 to the APM and LPM via the Ca2+/ cyclic guanosine monophosphate (cGMP)/PKG signaling pathway, which is associated with store-operated Ca2+ entry.
影响因子：
4
作者：
Pani B;Singh BB
通讯作者：
Singh BB
影响因子：
21.1
作者：
Kimberly A. Lucas;G. Pitari;G. Pitari;S. Kazerounian;I. Ruiz-Stewart;Jason Y. Park;S. Schulz;K. Chepenik;S. Waldman
通讯作者：
Kimberly A. Lucas;G. Pitari;G. Pitari;S. Kazerounian;I. Ruiz-Stewart;Jason Y. Park;S. Schulz;K. Chepenik;S. Waldman
大鼠腮腺腺泡细胞上的非典型 α-1 肾上腺素受体。
DOI：
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发表时间：
1992
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Porter,JE;Dowd,FJ;Abel,PW
通讯作者：
Abel,PW