Osmolytes and Mechanisms Involved in Regulatory Volume Decrease Under Conditions of Sudden or Gradual Osmolarity Decrease

Ordaz, Benito; Tuz, Karina; Ochoa, Lenin D.; Lezama, Ruth; Peña-Segura, Claudia; Franco, Rodrigo

doi:10.1023/b:nere.0000010434.06311.18

Cited by 37 publications

(30 citation statements)

References 38 publications

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“…Astrocytes are thought to be able to cope with brief exposures (30-90 min) to mild or moderate amounts of swelling by offloading osmolytes, including potentially excitotoxic neurotransmitters, a mechanism known as regulatory volume decrease (RVD) (Kimelberg 1987;Ordaz et al 2004;Thrane et al 2011;Anderova et al 2014). Conversely, hyperosmotic stress may be able to induce a regulatory volume increase (RVI) by uptake of osmolytes and water (Evanko et al 2004;Risher et al 2009).…”

Section: Astrocytes: Susceptible To Swellingmentioning

confidence: 99%

Brain edema: a valid endpoint for measuring hepatic encephalopathy?

Bémeur

Cudalbu

Dam³

et al. 2016

Metab Brain Dis

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Hepatic encephalopathy (HE) is a major complication of liver failure/disease which frequently develops during the progression of end-stage liver disease. This metabolic neuropsychiatric syndrome involves a spectrum of symptoms, including cognition impairment, attention deficits and motor dysfunction which eventually can progress to coma and death. Pathologically, HE is characterized by swelling of the astrocytes which consequently leads to brain edema, a common feature found in patients with acute liver failure (ALF) as well as in cirrhotic patients suffering from HE. The pathogenic factors involved in the onset of astrocyte swelling and brain edema in HE are unresolved. However, the role of astrocyte swelling/brain edema in the development of HE remains ambiguous and therefore measuring brain edema as an endpoint to evaluate HE is questioned. The following review will determine the effect of astrocyte swelling and brain edema on neurological function, discuss the various possible techniques to measure brain edema and lastly to propose a number of neurobehavioral tests to evaluate HE.

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Section: Astrocytes: Susceptible To Swellingmentioning

confidence: 99%

Brain edema: a valid endpoint for measuring hepatic encephalopathy?

Bémeur

Cudalbu

Dam³

et al. 2016

Metab Brain Dis

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“…Third, volume-activated taurine transport appears to 'inactivate' in the presence of a prolonged hyposmotic shock [23,28,42,43]: this is probably a reflection that cells are regulating their volume during the hyposmotic challenge. Fourth, an abrupt osmotic shock increases taurine efflux to a much greater extent than delivering the same osmotic challenge gradually [41,44]. Fifth, swelling-induced taurine efflux can also be reduced by lowering the temperature of the incubation buffer which is probably a consequence of interfering with signal transduction processes [22,41,42].…”

Section: General Characteristics Of Volumeactivated Taurine Releasementioning

confidence: 99%

Swelling-Induced Taurine Transport: Relationship with Chloride Channels, Anion-Exchangers and Other Swelling-Activated Transport Pathways

Shennan¹

2008

Cell Physiol Biochem

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Cells have to regulate their volume in order to survive. Moreover, it is now evident that cell volume per se and the membrane transport processes which regulate it, comprise an important signalling unit. For example, macromolecular synthesis, apoptosis, cell growth and hormone secretion are all influenced by the cellular hydration state. Therefore, a thorough understanding of volume-activated transport processes could lead to new strategies being developed to control the function and growth of both normal and cancerous cells. Cell swelling stimulates the release of ions such as K⁺ and Cl^- together with organic osmolytes, especially the β-amino acid taurine. Despite being the subject of intense research interest, the nature of the volume-activated taurine efflux pathway is still a matter of controversy. On the one hand it has been suggested that osmosensitive taurine efflux utilizes volume-sensitive anion channels whereas on the other it has been proposed that the band 3 anion-exchanger is a swelling-induced taurine efflux pathway. This article reviews the evidence for and against a role of anion channels and exchangers in osmosensitive taurine transport. Furthermore, the distinct possibility that neither pathway is involved in taurine transport is highlighted. The putative relationship between swelling-induced taurine transport and volume-activated anionic amino acid, α-neutral amino acid and K⁺ transport is also examined.

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“…After the swelling, cells can return to their original volume through a complex mechanism called regulatory volume decrease (RVD). This process is based on the efflux of ions (usually ClϪ and Kϩ) and osmolytes followed by water efflux along the osmotic gradient (2)(3)(4). In contrast, in response to an increase in extracellular osmolality, cells shrink and eventually regain their original volume in a complex mechanism known as regulatory volume increase (RVI).…”

mentioning

confidence: 99%

Hypotonicity Induces Aquaporin-2 Internalization and Cytosol-to-Membrane Translocation of ICln in Renal Cells

et al. 2007

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Kidney collecting-duct cells swell in response to changes in medulla osmolality caused by the transition from antidiuresis to diuresis. Regulatory volume decrease (RVD) mechanisms must be activated to face this hypotonic stress. In Aquaporin-2 (AQP2)-expressing renal CD8 cells, hypotonicity decreased cell surface expression of AQP2 and increased the amount of AQP2 localized intracellularly, whereas the total amount of AQP2 phosphorylated at ser-256 decreased. Analysis of cAMP dynamics using fluorescence resonance energy transfer (FRET) showed that hypotonicity causes a reduction of cAMP, consistent with a decrease in phospho-AQP2. Moreover, hypotonicity caused a profound actin reorganization, associated with the loss of stress fibers and formation of F-actin patches (microspikes) at the cell border. Those changes were regulated by the monomeric GTPase Cdc42. Interestingly, expression of the dominant-negative Cdc42 (N17-Cdc42) prevented the hypotonicity-induced microspike formation and the generation of Cl(-) currents. Hypotonicity also caused the relocation from the cytosol to the plasma membrane and increase in interaction with actin of ICln (nucleotide-sensitive chloride current protein), which is essential for the generation of ion currents activated during RVD. Together, the profound actin remodeling, internalization of AQP2 and translocation of ICln to the plasma membrane during hypotonicity may contribute to RVD after cell swelling in renal medulla.

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Osmolytes and Mechanisms Involved in Regulatory Volume Decrease Under Conditions of Sudden or Gradual Osmolarity Decrease

Cited by 37 publications

References 38 publications

Brain edema: a valid endpoint for measuring hepatic encephalopathy?

Brain edema: a valid endpoint for measuring hepatic encephalopathy?

Swelling-Induced Taurine Transport: Relationship with Chloride Channels, Anion-Exchangers and Other Swelling-Activated Transport Pathways

Hypotonicity Induces Aquaporin-2 Internalization and Cytosol-to-Membrane Translocation of ICln in Renal Cells

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