Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

Park, Jae-Seung; Choi, Yong Jin; Siegrist, Vicki J.; Ko, Yoo-Seung; Cho, Won Kyoo

doi:10.1007/s00424-007-0274-7

Cited by 9 publications

(5 citation statements)

References 48 publications

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“…This is consistent with previous reports that the activation of VRAC does not require an increase of intracellular Ca 2ϩ (37,77). However, there is considerable evidence that although elevation of Ca 2ϩ is not necessary, a low level of Ca 2ϩ (ϳ50 -100 nM) is required for VRAC activation, at least in certain cell types (25,147,155,197). hBest1 has an EC 50 for Ca 2ϩ of ϳ150 nM, which is very close to the permissive level for VRAC activation.…”

Section: B Volume Sensitivity Of Bestrophinssupporting

confidence: 91%

Molecular Physiology of Bestrophins: Multifunctional Membrane Proteins Linked to Best Disease and Other Retinopathies

Hartzell¹,

Qu²,

Yu³

et al. 2008

Physiological Reviews

306

393

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This article reviews the current state of knowledge about the bestrophins, a newly identified family of proteins that can function both as Cl(-) channels and as regulators of voltage-gated Ca(2+) channels. The founding member, human bestrophin-1 (hBest1), was identified as the gene responsible for a dominantly inherited, juvenile-onset form of macular degeneration called Best vitelliform macular dystrophy. Mutations in hBest1 have also been associated with a small fraction of adult-onset macular dystrophies. It is proposed that dysfunction of bestrophin results in abnormal fluid and ion transport by the retinal pigment epithelium, resulting in a weakened interface between the retinal pigment epithelium and photoreceptors. There is compelling evidence that bestrophins are Cl(-) channels, but bestrophins remain enigmatic because it is not clear that the Cl(-) channel function can explain Best disease. In addition to functioning as a Cl(-) channel, hBest1 also is able to regulate voltage-gated Ca(2+) channels. Some bestrophins are activated by increases in intracellular Ca(2+) concentration, but whether bestrophins are the molecular counterpart of Ca(2+)-activated Cl(-) channels remains in doubt. Bestrophins are also regulated by cell volume and may be a member of the volume-regulated anion channel family.

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Section: B Volume Sensitivity Of Bestrophinssupporting

confidence: 91%

Molecular Physiology of Bestrophins: Multifunctional Membrane Proteins Linked to Best Disease and Other Retinopathies

Hartzell¹,

Qu²,

Yu³

et al. 2008

Physiological Reviews

306

393

View full text Add to dashboard Cite

show abstract

“…This is consistent with previous reports that the activation of VRAC does not require an increase of intracellular Ca 2+ (Hazama and Okada, 1988;Doroshenko and Neher, 1992). However, there is considerable evidence that although elevation of Ca 2+ is not necessary, a low level of Ca 2+ ‫001-05ف(‬ nM) is required for VRAC activation, at least in certain cell types (Szucs et al, 1996;Nilius et al, 1997;Altamirano et al, 1998;Chen et al, 2007;Park et al, 2007). hBest1 has an EC 50 for Ca 2+ of ‫051ف‬ nM, which is very close to the permissive level for VRAC activation.…”

Section: Similarities and Differences Between Classical Vrac And S2 Vracsupporting

confidence: 91%

DrosophilaBestrophin-1 Chloride Current Is Dually Regulated by Calcium and Cell Volume

Chien¹,

Hartzell²

2007

J Cell Biol

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Mutations in the human bestrophin-1 (hBest1) gene are responsible for Best vitelliform macular dystrophy, however the mechanisms leading to retinal degeneration have not yet been determined because the function of the bestrophin protein is not fully understood. Bestrophins have been proposed to comprise a new family of Cl − channels that are activated by Ca 2+ . While the regulation of bestrophin currents has focused on intracellular Ca 2+ , little is known about other pathways/mechanisms that may also regulate bestrophin currents. Here we show that Cl − currents in Drosophila S2 cells, that we have previously shown are mediated by bestrophins, are dually regulated by Ca 2+ and cell volume. The bestrophin Cl − currents were activated in a dose-dependent manner by osmotic pressure differences between the internal and external solutions. The increase in the current was accompanied by cell swelling. The volume-regulated Cl − current was abolished by treating cells with each of four different RNAi constructs that reduced dBest1 expression. The volume-regulated current was rescued by transfecting with dBest1. Furthermore, cells not expressing dBest1 were severely depressed in their ability to regulate their cell volume. Volume regulation and Ca 2+ regulation can occur independently of one another: the volume-regulated current was activated in the complete absence of Ca 2+ and the Ca 2+ -activated current was activated independently of alterations in cell volume. These two pathways of bestrophin channel activation can interact; intracellular Ca 2+ potentiates the magnitude of the current activated by changes in cell volume. We conclude that in addition to being regulated by intracellular Ca 2+ , Drosophila bestrophins are also novel members of the volume-regulated anion channel (VRAC) family that are necessary for cell volume homeostasis.

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“…However, in most cases, GPCR agonist-induced potentiation of intracellular Ca 2þ rise increases the efflux of these osmolytes, an effect that is also mimicked by the use of Ca 2þ -ionophores (Junankar et al, 2002;Mongin andKimelberg, 2002, 2005;Cardin et al, 2003;Loveday et al, 2003;Franco et al, 2004b). These results, together with the observation that a permissive Ca 2þ concentration is necessary for both RVD and the activation of Cl À /organic osmolyte release (Szucs et al, 1996;Mongin et al, 1999;Park et al, 2007), suggest a regulatory role for intracellular Ca 2þ in the activation of these pathways. The mechanisms involved in this phenomenon are still unclear, however, a recent report by Falktoft and Lambert (2004) showed that agonist-induced increase in intracellular Ca 2þ prior to the induction of cell swelling still potentiates RVD and osmolyte efflux, even though the intracellular Ca 2þ concentration has already returned to basal conditions at the moment of the swelling-induced stimulus.…”

Section: Membrane Receptors As Cell Volume Sensorsmentioning

confidence: 84%

Autocrine signaling involved in cell volume regulation: The role of released transmitters and plasma membrane receptors

Franco

Panayiotidis

Paz

2008

Journal Cellular Physiology

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Cell volume regulation is a basic homeostatic mechanism transcendental for the normal physiology and function of cells. It is mediated principally by the activation of osmolyte transport pathways that result in net changes in solute concentration that counteract cell volume challenges in its constancy. This process has been described to be regulated by a complex assortment of intracellular signal transduction cascades. Recently, several studies have demonstrated that alterations in cell volume induce the release of a wide variety of transmitters including hormones, ATP and neurotransmitters, which have been proposed to act as extracellular signals that regulate the activation of cell volume regulatory mechanisms. In addition, changes in cell volume have also been reported to activate plasma membrane receptors (including tyrosine kinase receptors, G-protein coupled receptors and integrins) that have been demonstrated to participate in the regulatory process of cell volume. In this review, we summarize recent studies about the role of changes in cell volume in the regulation of transmitter release as well as in the activation of plasma membrane receptors and their further implications in the regulation of the signaling machinery that regulates the activation of osmolyte flux pathways. We propose that the autocrine regulation of Ca2+-dependent and tyrosine phosphorylation-dependent signaling pathways by the activation of plasma membrane receptors and swelling-induced transmitter release is necessary for the activation/regulation of osmolyte efflux pathways and cell volume recovery. Furthermore, we emphasize the importance of studying these extrinsic signals because of their significance in the understanding of the physiology of cell volume regulation and its role in cell biology in vivo, where the constraint of the extracellular space might enhance the autocrine or even paracrine signaling induced by these released transmitters.

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Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

Cited by 9 publications

References 48 publications

Molecular Physiology of Bestrophins: Multifunctional Membrane Proteins Linked to Best Disease and Other Retinopathies

Molecular Physiology of Bestrophins: Multifunctional Membrane Proteins Linked to Best Disease and Other Retinopathies

DrosophilaBestrophin-1 Chloride Current Is Dually Regulated by Calcium and Cell Volume

Autocrine signaling involved in cell volume regulation: The role of released transmitters and plasma membrane receptors

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