Functional interaction between AQP2 and TRPV4 in renal cells

We have previously demonstrated that renal cortical collecting duct cells (RCCD1), responded to hypotonic stress with a rapid activation of regulatory volume decrease (RVD) mechanisms. This process requires the presence of the water channel AQP2 and calcium influx, opening the question about the mol...

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Bibliographic Details
Published in:Journal of cellular biochemistry 2012-02, Vol.113 (2), p.580-589
Main Authors: Galizia, Luciano, Pizzoni, Alejandro, Fernandez, Juan, Rivarola, Valeria, Capurro, Claudia, Ford, Paula
Format: Article
Language:English
Subjects:
Animals
AQUAPORIN 2
Aquaporin 2 - metabolism
Calcium Channel Blockers - pharmacology
Calcium Signaling - drug effects
Capsaicin - pharmacology
Cell Size
CELL VOLUME REGULATION
Cells, Cultured
Cytochalasin D - pharmacology
Cytoskeleton - drug effects
Cytoskeleton - metabolism
Gene Expression
INTRACELLULAR CALCIUM
Kidney - cytology
Osmotic Pressure
Phorbols - pharmacology
Protein Binding
Protein Transport
Rats
Ruthenium Red - pharmacology
Stress, Physiological
TRANSIENT RECEPTOR POTENTIAL VANILLOID 4
TRPV Cation Channels - agonists
TRPV Cation Channels - genetics
TRPV Cation Channels - metabolism
Tubulin Modulators - pharmacology
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Summary:We have previously demonstrated that renal cortical collecting duct cells (RCCD1), responded to hypotonic stress with a rapid activation of regulatory volume decrease (RVD) mechanisms. This process requires the presence of the water channel AQP2 and calcium influx, opening the question about the molecular identity of this calcium entry path. Since the calcium permeable nonselective cation channel TRPV4 plays a crucial role in the response to mechanical and osmotic perturbations in a wide range of cell types, the aim of this work was to test the hypothesis that the increase in intracellular calcium concentration and the subsequent rapid RVD, only observed in the presence of AQP2, could be due to a specific activation of TRPV4. We evaluated the expression and function of TRPV4 channels and their contribution to RVD in WT‐RCCD1 (not expressing aquaporins) and in AQP2‐RCCD1 (transfected with AQP2) cells. Our results demonstrated that both cell lines endogenously express functional TRPV4, however, a large activation of the channel by hypotonicity only occurs in cells that express AQP2. Blocking of TRPV4 by ruthenium red abolished calcium influx as well as RVD, identifying TRPV4 as a necessary component in volume regulation. Even more, this process is dependent on the translocation of TRPV4 to the plasma membrane. Our data provide evidence of a novel association between TRPV4 and AQP2 that is involved in the activation of TRPV4 by hypotonicity and regulation of cellular response to the osmotic stress, suggesting that both proteins are assembled in a signaling complex that responds to anisosmotic conditions. J. Cell. Biochem. 113: 580–589, 2012. © 2011 Wiley Periodicals, Inc.
ISSN:0730-2312
1097-4644
DOI:10.1002/jcb.23382