1. Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions
- Author
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Di Wang, Masayuki Shono, Yasuko Ishikawa, Aneta M. Bragiel, and Tomasz D. Pieczonka
- Subjects
0301 basic medicine ,Male ,aquaporin-5 ,Acinar Cells ,Cell membrane ,lcsh:Chemistry ,protein G kinase ,chemistry.chemical_compound ,hypotonicity ,Phenylephrine ,α1B-adrenoceptor ,Parotid Gland ,lcsh:QH301-705.5 ,Spectroscopy ,General Medicine ,Immunohistochemistry ,Computer Science Applications ,Cell biology ,Protein Transport ,medicine.anatomical_structure ,Hypotonic Solutions ,Signal transduction ,medicine.medical_specialty ,Ruthenium red ,G(M1) Ganglioside ,Biology ,Catalysis ,Article ,Nitric oxide ,Inorganic Chemistry ,03 medical and health sciences ,α1A-adrenoceptor ,Internal medicine ,Receptors, Adrenergic, alpha-1 ,medicine ,Extracellular ,Animals ,Secretion ,Physical and Theoretical Chemistry ,Rats, Wistar ,Protein kinase A ,α1D-adrenoceptor ,calcium ,Phentolamine ,Molecular Biology ,Cyclic guanosine monophosphate ,Organic Chemistry ,Cell Membrane ,Aquaporin 5 ,Rats ,030104 developmental biology ,Endocrinology ,chemistry ,lcsh:Biology (General) ,lcsh:QD1-999 ,Adrenergic alpha-1 Receptor Antagonists ,Adrenergic alpha-1 Receptor Agonists ,Isotonic Solutions - 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 La(3+), implying the participation of store-operated Ca(2+) 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 La(3+), suggesting the involvement of extracellular Ca(2+) entry. Thus, α1A-AR activation induced the trafficking of AQP5 to the APM and LPM via the Ca(2+)/ cyclic guanosine monophosphate (cGMP)/PKG signaling pathway, which is associated with store-operated Ca(2+) entry.
- Published
- 2016