Role of AQP2 in activation of calcium entry by hypotonicity: implications in cell volume regulation

Galizia, Luciano; Flamenco, María del Pilar; Rivarola, Valeria; Capurro, Claudia; Ford, Paula

doi:10.1152/ajprenal.00427.2007

Cited by 34 publications

(30 citation statements)

References 57 publications

(69 reference statements)

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“…] osmotic shrinkage/swelling also varies between cell types, being very high in EAT cells (see Fig. 1) and low in, e.g., rat cortical collecting duct cells (264). From the scanning electron micrographs in Figure 1, it is seen that the initial increase/decrease in cell volume involves unfolding/folding of the plasma membrane.…”

Section: Cell Volume Regulationmentioning

confidence: 94%

“…As detailed below, the osmotic water permeability of animal cells is several orders of magnitude greater than the permeability towards Na ϩ , K ϩ , and Cl Ϫ . In many cell types, a high water permeability reflects the presence of aquaporins (AQPs), and it has been shown that the presence of AQP2 (cortical collecting duct cells) or AQP5 (salivary gland cells) dramatically increases the rate of initial cell swelling following hypotonic exposure (264,579). For a detailed description of the physiology of AQPs, see Reference 448.…”

Section: Introductionmentioning

confidence: 99%

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Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,302

1,677

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The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K+, Cl−, and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na+/H+exchange, Na+-K+-2Cl−cotransport, and Na+channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca2+, protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.

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Section: Cell Volume Regulationmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,302

1,677

View full text Add to dashboard Cite

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“…We also established that this RVD is related to the activation of the cystic fibrosis transmembrane conductance regulator (CFTR) and to barium-sensitive potassium channels [Ford et al, 2005] causing the exit of K the intracellular calcium concentration ([Ca 2þ ] i ) that only occurs in the presence of AQP2 [Galizia et al, 2008]. In fact, wild-type cells not expressing AQP2 (WT-RCCD 1 ) showed a diminutive increase in [Ca 2þ ] i and were incapable of producing a rapid activation of RVD.…”

mentioning

confidence: 96%

Functional interaction between AQP2 and TRPV4 in renal cells

Galizia¹,

Pizzoni²,

Fernández³

et al. 2012

J of Cellular Biochemistry

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We have previously demonstrated that renal cortical collecting duct cells (RCCD 1 ), 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-RCCD 1 (not expressing aquaporins) and in AQP2-RCCD 1 (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. ß 2011 Wiley Periodicals, Inc.KEY WORDS: AQUAPORIN 2; TRANSIENT RECEPTOR POTENTIAL VANILLOID 4; CELL VOLUME REGULATION; INTRACELLULAR CALCIUM M any cell types have evolved specialized mechanisms of volume regulation to counteract damage induced by either cell swelling or shrinking. Under hypotonic conditions, cells first respond by swelling and second by initiating a mechanism that allows them to recover their original volume, this mechanism is called regulatory volume decrease (RVD) [O'Neill, 1999;Okada et al., 2001;Lang, 2007]. Essentially all cells respond to hypotonic swelling with this complex mechanism but the response is usually incomplete probably due to the fact that a new steady-state volume is achieved [O'Neill, 1999]. RVD depends on the release of inorganic and organic osmolytes that reverse the osmotic gradient and direction of water flow [Okada et al., 2001;Strange, 2004;Lang, 2007]. A number of ion channels and transporters were identified as the pathways for volume-regulatory ionic flux [Lang, 2007], however, the underlying mechanism that senses the change in osmolarity and/or cell volume to initiate volume regulation is not yet completely understood.We have previously demonstrated, in a rat cortical collecting duct cell line (RCCD 1 ) which exhibits many major functional properties of the cortical collecting duct (CCD) [Blot-Chabaud et al., 1996;Dje...

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“…In astrocytes and retinal Muller cells, TRPV4 is functionally linked to AQP4 (Benfenati et al, 2011;Jo et al, 2015), and this association is a requirement for RVD. TRPV4 associates with AQP5 in acinar and salivary gland cells (Liu et al, 2006;Hosoi, 2016) and with AQP2 in renal cells (Galizia et al, 2008).…”

mentioning

confidence: 99%

Channels and Volume Changes in the Life and Death of the Cell

Pasantes‐Morales

2016

Mol Pharmacol

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Volume changes deviating from original cell volume represent a major challenge for cellular homeostasis. Cell volume may be altered either by variations in the external osmolarity or by disturbances in the transmembrane ion gradients that generate an osmotic imbalance. Cells respond to anisotonicity-induced volume changes by active regulatory mechanisms that modify the intracellular/extracellular concentrations of K 1 , Cl -, Na 1 , and organic osmolytes in the direction necessary to reestablish the osmotic equilibrium. Corrective osmolyte fluxes permeate across channels that have a relevant role in cell volume regulation. Channels also participate as causal actors in necrotic swelling and apoptotic volume decrease. This is an overview of the types of channels involved in either corrective or pathologic changes in cell volume. The review also underlines the contribution of transient receptor potential (TRP) channels, notably TRPV4, in volume regulation after swelling and describes the role of other TRPs in volume changes linked to apoptosis and necrosis. Lastly we discuss findings showing that multimers derived from LRRC8A (leucine-rich repeat containing 8A) gene are structural components of the volume-regulated Cl -channel (VRAC), and we underline the intriguing possibility that different heteromer combinations comprise channels with different intrinsic properties that allow permeation of the heterogenous group of molecules acting as organic osmolytes.

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Role of AQP2 in activation of calcium entry by hypotonicity: implications in cell volume regulation

Cited by 34 publications

References 57 publications

Physiology of Cell Volume Regulation in Vertebrates

Physiology of Cell Volume Regulation in Vertebrates

Functional interaction between AQP2 and TRPV4 in renal cells

Channels and Volume Changes in the Life and Death of the Cell

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