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Int. J. Mol. Sci. 2016, 17(7), 1022; doi:10.3390/ijms17071022

Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions

1
Department of Medical Pharmacology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8504, Japan
2
Support Center for Advanced Medical Sciences, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8504, Japan
Present address: Department of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China
*
Author to whom correspondence should be addressed.
Academic Editor: Kenichi Ishibashi
Received: 20 April 2016 / Revised: 15 June 2016 / Accepted: 23 June 2016 / Published: 28 June 2016
(This article belongs to the Special Issue Aquaporin)
View Full-Text   |   Download PDF [5885 KB, uploaded 28 June 2016]   |  

Abstract

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. View Full-Text
Keywords: aquaporin-5; α1A-adrenoceptor; α1B-adrenoceptor; α1D-adrenoceptor; calcium; protein G kinase; hypotonicity aquaporin-5; α1A-adrenoceptor; α1B-adrenoceptor; α1D-adrenoceptor; calcium; protein G kinase; hypotonicity
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MDPI and ACS Style

Bragiel, A.M.; Wang, D.; Pieczonka, T.D.; Shono, M.; Ishikawa, Y. Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions. Int. J. Mol. Sci. 2016, 17, 1022.

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