Dual Effects of Hypertonicity on Aquaporin-2 Expression in Cultured Renal Collecting Duct Principal Cells

Hasler, Udo; Vinciguerra, Manlio; Vandewalle, Alain; Martin, Pierre‐Yves; Féraille, Eric

doi:10.1681/asn.2004110930

Cited by 84 publications

(92 citation statements)

References 43 publications

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“…Hyperosmolality has been shown to upregulate AQP2 in several in vitro cell culture systems (7,8), but, to date, the effect of increased osmolality in vivo to enhance AQP2 protein expression and trafficking remains to be documented clearly. In this regard, there have been conflicting results about the effects of fluid deprivation in BB rats to alter AQP2 expression (19,22).…”

Section: Discussionmentioning

confidence: 99%

“…Hyperosmolality also increased the expression of AQP3 in vitro (6). In recent in vitro studies, a long-term (24 h) increase of extracellular tonicity by addition of NaCl or sucrose increased AQP2 expression via stimulation of AQP2 gene transcription (7). In mouse inner medullary CD mIMCD3 cell lines that were transfected with AQP2 cDNA, hyperosmolality with supplemented NaCl increased the expression of nonglycosylated AQP2 and enhanced the apical membrane insertion of nonglycosylated AQP2 in the absence of AVP.…”

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confidence: 84%

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Hyperosmolality In Vivo Upregulates Aquaporin 2 Water Channel and Na-K-2Cl Co-Transporter in Brattleboro Rats

Wang²,

Summer³

et al. 2006

Journal of the American Society of Nephrology

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There are considerable experimental results that indicate that arginine vasopressin (AVP)-independent factors are involved in urinary concentration. This study examined the role of hyperosmolality in vivo to modulate aquaporin 2 (AQP2) and Na-K-2Cl co-transporter (NKCC2), pivotal factors in urinary concentration, in AVP-deficient Brattleboro (BB) rats. Hyperglycemia with associated hyperosmolality occurred in diabetic BB rats (BBDM). Protein abundance of AQP2 increased and was reversed by insulin in the inner medulla (IM; control 100 ؎ 5%; BBDM 146 ؎ 8%; BBDM؉Ins 122 ؎ 9%; P < 0.001) and inner stripe of outer medulla (ISOM; control 100 ؎ 4%; BBDM 123 ؎ 8%; BBDM؉Ins 93 ؎ 6%; P < 0.05). These results were confirmed by immunohistochemistry studies. NKCC2 rose in the ISOM but was not reversed with insulin treatment. For investigation of the role of hyperosmolality in the absence of hyperglycemia on the regulation of the expression of renal AQP and NKCC2, studies were performed with hyperosmolality that was induced by 0.5% NaCl in drinking water in BB rats. Hyperosmolality that was induced by NaCl increased significantly the protein abundance of IM AQP2 (121 ؎ 2 versus 100 ؎ 5%; P < 0.01), ISOM AQP2 (135 ؎ 6 versus 100 ؎ 5%; P < 0.001), cortex plus outer stripe of outer medulla AQP2 (121 ؎ 4 versus 100 ؎ 1%; P < 0.001), ISOM NKCC2 (133 ؎ 1 versus 100 ؎ 4%; P < 0.05), and cortex plus outer stripe of outer medulla NKCC2 (142 ؎ 16 versus 100 ؎ 9%; P < 0.05). In conclusion, hyperosmolality, secondary to either glucose or NaCl, upregulated renal AQP2 and NKCC2 in vivo in BB rats.J Am Soc Nephrol 17: 1657 -1664, 2006 . doi: 10.1681 R enal water excretion is regulated by arginine vasopressin (AVP), which increases the water permeability in the collecting duct (CD) (1,2). Recently, the water channel aquaporin 2 (AQP2) that mediates the water transport in the CD in response to vasopressin was identified (3). It is widely known that AQP2 is the main target for the action of vasopressin to regulate CD water reabsorption and hence body water balance via the V 2 receptor and cAMP pathway (4).There is, however, some in vitro evidence for vasopressinindependent effects on the regulation of water channels. For example, it has been demonstrated that hypertonicity enhances the expression and the stability of AQP1 in the absence of AVP in cultured murine renal medullary cells (5). Hyperosmolality also increased the expression of AQP3 in vitro (6). In recent in vitro studies, a long-term (24 h) increase of extracellular tonicity by addition of NaCl or sucrose increased AQP2 expression via stimulation of AQP2 gene transcription (7). In mouse inner medullary CD mIMCD3 cell lines that were transfected with AQP2 cDNA, hyperosmolality with supplemented NaCl increased the expression of nonglycosylated AQP2 and enhanced the apical membrane insertion of nonglycosylated AQP2 in the absence of AVP. These results indicate that hyperosmolality may play a critical role in the regulation of AQP2 in the CD (8). Taken together, these in vitro studies s...

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Section: Discussionmentioning

confidence: 99%

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confidence: 84%

Hyperosmolality In Vivo Upregulates Aquaporin 2 Water Channel and Na-K-2Cl Co-Transporter in Brattleboro Rats

Wang²,

Summer³

et al. 2006

Journal of the American Society of Nephrology

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“…Cell lysates were prepared and quantified as described previously (78). Actin polymerization was quantified by determining the Triton X-100-soluble (G-actin)/TritonX-100-insoluble (F-actin) ratio.…”

Section: Measurement Of Relative Changes In [Clmentioning

confidence: 99%

Ionic imbalance, in addition to molecular crowding, abates cytoskeletal dynamics and vesicle motility during hypertonic stress

Nunes

Roth

Meda

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Cell volume homeostasis is vital for the maintenance of optimal protein density and cellular function. Numerous mammalian cell types are routinely exposed to acute hypertonic challenge and shrink. Molecular crowding modifies biochemical reaction rates and decreases macromolecule diffusion. Cell volume is restored rapidly by ion influx but at the expense of elevated intracellular sodium and chloride levels that persist long after challenge. Although recent studies have highlighted the role of molecular crowding on the effects of hypertonicity, the effects of ionic imbalance on cellular trafficking dynamics in living cells are largely unexplored. By tracking distinct fluorescently labeled endosome/vesicle populations by live-cell imaging, we show that vesicle motility is reduced dramatically in a variety of cell types at the onset of hypertonic challenge. Live-cell imaging of actin and tubulin revealed similar arrested microfilament motility upon challenge. Vesicle motility recovered long after cell volume, a process that required functional regulatory volume increase and was accelerated by a return of extracellular osmolality to isosmotic levels. This delay suggests that, although volume-induced molecular crowding contributes to trafficking defects, it alone cannot explain the observed effects. Using fluorescent indicators and FRET-based probes, we found that intracellular ATP abundance and mitochondrial potential were reduced by hypertonicity and recovered after longer periods of time. Similar to the effects of osmotic challenge, isovolumetric elevation of intracellular chloride concentration by ionophores transiently decreased ATP production by mitochondria and abated microfilament and vesicle motility. These data illustrate how perturbed ionic balance, in addition to molecular crowding, affects membrane trafficking.electrolyte | cell volume | hypertonicity | membrane trafficking | mitochondria

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“…Hypertonicity has also been shown to trigger the translocation of AQPs 1, 2, 3, 4, 5 and 9 (Arima et al, 2003, Hasler et al, 2005, Hoffert et al, 2000, Loitto et al, 2007, Matsuzaki et al, 2001) whilst hypotonicity has been shown to be involved in translocation of AQPs 1, 3 and 8 (Conner et al, 2012, Conner et al, 2010, Garcia et al, 2011, Qi et al, 2009 (Table 2).…”

Section: What Triggers Aqp Translocation?mentioning

confidence: 99%

An emerging consensus on aquaporin translocation as a regulatory mechanism

Conner

Bill

Conner

2012

Molecular Membrane Biology

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Water can pass through the cell membrane relatively slowly by diffusion. However, in order to maintain water homeostasis, the rapid and specific regulation of cellular water flow is mediated by the aquaporin (AQP) family of membrane protein water channels. Thirteen human AQPs have been identified to date and the majority are highly specific for water while others show selectivity for water, glycerol and other small solutes. The wide range of tissues that are known to express AQPs is reflected by their involvement in many physiological processes and diseases. Receptor mediated translocation, via hormone activation, is an established method of AQP regulation, especially for AQP2. There is now an emerging consensus that the rapid and reversible translocation of other AQPs from intracellular vesicles to the plasma membrane, triggered by a range of stimuli, can confer increased membrane permeability. This review examines new advances that have identified molecular mechanisms of AQP regulation; these include the role of cytoskeletal proteins, kinases, calcium and retention or localisation signals as well as specific triggers of AQP translocation. This article reviews current knowledge of AQP regulation with a focus on rapid and dynamic regulation of sub-cellular AQP translocation in response to a specific trigger.3

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Dual Effects of Hypertonicity on Aquaporin-2 Expression in Cultured Renal Collecting Duct Principal Cells

Cited by 84 publications

References 43 publications

Hyperosmolality In Vivo Upregulates Aquaporin 2 Water Channel and Na-K-2Cl Co-Transporter in Brattleboro Rats

Hyperosmolality In Vivo Upregulates Aquaporin 2 Water Channel and Na-K-2Cl Co-Transporter in Brattleboro Rats

Ionic imbalance, in addition to molecular crowding, abates cytoskeletal dynamics and vesicle motility during hypertonic stress

An emerging consensus on aquaporin translocation as a regulatory mechanism

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