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Cell Physiol Biochem. 2019;53(4):687-700. doi: 10.33594/000000165.

Apelin-13 Regulates Vasopressin-Induced Aquaporin-2 Expression and Trafficking in Kidney Collecting Duct Cells.

Author information

1
Department of Pharmacology & Physiology, Faculty of Medicine and Health Sciences, Sherbrooke University, Sherbrooke, QC, Canada.
2
Department of Pathology, Faculty of Medicine and Health Sciences, Sherbrooke University, Sherbrooke, QC, Canada.
3
Department of Surgery, Faculty of Medicine and Health Sciences, Sherbrooke University, Sherbrooke, QC, Canada.
4
Research Center of the Centre Hospitalier Universitaire de Sherbrooke (CR-CHUS), Sherbrooke University, Sherbrooke, QC, Canada.
5
Department of Medicine, Faculty of Medicine and Health Sciences, Sherbrooke University, QC, Canada.
6
Research Center of the Centre Hospitalier Universitaire de Sherbrooke (CR-CHUS), Sherbrooke University, Sherbrooke, QC, Canada, Ahmed.chraibi@usherbrooke.ca.

Abstract

BACKGROUND/AIMS:

Apelin and its G protein-coupled receptor APJ (gene symbol Aplnr) are strongly expressed in magnocellular vasopressinergic neurons suggesting that the apelin/APJ system plays a key role at the central level in regulating salt and water balance by counteracting the antiduretic action of vasopressin (AVP). Likewise, recent studies revealed that apelin exerts opposite effects to those of vasopressin induced on water reabsorption via a direct action on the kidney collecting duct. However, the underlying mechanisms of the peripheral action of apelin are not clearly understood. Here, we thus investigated the role of the apelin/APJ system in the regulation of water balance in the kidney, and more specifically its involvement in modulating the function of aquaporin-2 (AQP2) in the collecting duct.

METHODS:

Mouse cortical collecting duct cells (mpkCCD) were incubated in the presence of dDAVP and treated with or without apelin-13. Changes in AQP2 expression and localization were determined by immunoblotting and confocal immunofluorescence staining.

RESULTS:

Herein, we showed that the APJ was present in mpkCCD cells. Treatment of mpkCCD with apelin-13 reduced the cAMP production and antagonized the AVP-induced increase in AQP2 mRNA and protein expressions. Immunofluorescent experiments also revealed that the AVP-induced apical cell surface expression of AQP2, and notably its phosphorylated isoform AQP2-pS269, was considerably reduced following apelin-13 application to mpkCCD cells.

CONCLUSION:

Our data reinforce the aquaretic role of the apelin/APJ system in the fine regulation of body fluid homeostasis at the kidney level and its physiological opposite action to the antiduretic activity of AVP.

KEYWORDS:

Apelin; Aquaporin; Confocal microscopy; Kidney; PCR; Vasopressin; mpkCCD

PMID:
31577078
DOI:
10.33594/000000165
[Indexed for MEDLINE]
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