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      Distinct contributions of LRRC8A and its paralogs to the VSOR anion channel from those of the ASOR anion channel

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          ABSTRACT

          Volume- and acid-sensitive outwardly rectifying anion channels (VSOR and ASOR) activated by swelling and acidification exhibit voltage-dependent inactivation and activation time courses, respectively. Recently, LRRC8A and some paralogs were shown to be essentially involved in the activity and inactivation kinetics of VSOR currents in human colonic HCT116 cells. In human cervix HeLa cells, here, inactivation of VSOR currents was found to become accelerated by RNA silencing only of LRRC8A but never decelerated by that of any LRRC8 isoform. These data suggest that LRRC8A is associated with the deceleration mechanism of VSOR inactivation, while none of LRRC8 members is related to the acceleration mechanism. Activation kinetics of ASOR currents was unaffected by knockdown of any LRRC8 family member. Double, triple and quadruple gene-silencing studies indicated that combinatory expression of LRRC8A with LRRC8D and LRRC8C is essential for VSOR activity, whereas none of LRRC8 family members is involved in ASOR activity.

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          Physiology of cell volume regulation in vertebrates.

          Else K. Hoffmann, Ian H. Lambert, Stine F. Pedersen (2009)
          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, Ca(2+), 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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            SWELL1, a plasma membrane protein, is an essential component of volume-regulated anion channel.

            Zhaozhu Qiu, Adrienne E. Dubin, Jayanti Mathur … (2014)
            Maintenance of a constant cell volume in response to extracellular or intracellular osmotic changes is critical for cellular homeostasis. Activation of a ubiquitous volume-regulated anion channel (VRAC) plays a key role in this process; however, its molecular identity in vertebrates remains unknown. Here, we used a cell-based fluorescence assay and performed a genome-wide RNAi screen to find components of VRAC. We identified SWELL1 (LRRC8A), a member of a four-transmembrane protein family with unknown function, as essential for hypotonicity-induced iodide influx. SWELL1 is localized to the plasma membrane, and its knockdown dramatically reduces endogenous VRAC currents and regulatory cell volume decrease in various cell types. Furthermore, point mutations in SWELL1 cause a significant change in VRAC anion selectivity, demonstrating that SWELL1 is an essential VRAC component. These findings enable further molecular characterization of the VRAC channel complex and genetic studies for understanding the function of VRAC in normal physiology and disease. Copyright © 2014 Elsevier Inc. All rights reserved.
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              Receptor-mediated control of regulatory volume decrease (RVD) and apoptotic volume decrease (AVD).

              Vitoria T. Shimizu, E Maeno, K Dezaki … (2001)
              A fundamental property of animal cells is the ability to regulate their own cell volume. Even under hypotonic stress imposed by either decreased extracellular or increased intracellular osmolarity, the cells can re-adjust their volume after transient osmotic swelling by a mechanism known as regulatory volume decrease (RVD). In most cell types, RVD is accomplished mainly by KCl efflux induced by parallel activation of K+ and Cl- channels. We have studied the molecular mechanism of RVD in a human epithelial cell line (Intestine 407). Osmotic swelling results in a significant increase in the cytosolic Ca2+ concentration and thereby activates intermediate-conductance Ca2+-dependent K+ (IK) channels. Osmotic swelling also induces ATP release from the cells to the extracellular compartment. Released ATP stimulates purinergic ATP (P2Y2) receptors, thereby inducing phospholipase C-mediated Ca2+ mobilization. Thus, RVD is facilitated by stimulation of P2Y2 receptors due to augmentation of IK channels. In contrast, stimulation of another G protein-coupled Ca2+-sensing receptor (CaR) enhances the activity of volume-sensitive outwardly rectifying Cl- channels, thereby facilitating RVD. Therefore, it is possible that Ca2+ efflux stimulated by swelling-induced and P2Y2 receptor-mediated intracellular Ca2+ mobilization activates the CaR, thereby secondarily upregulating the volume-regulatory Cl- conductance. On the other hand, the initial process towards apoptotic cell death is coupled to normotonic cell shrinkage, called apoptotic volume decrease (AVD). Stimulation of death receptors, such as TNF receptor and Fas, induces AVD and thereafter biochemical apoptotic events in human lymphoid (U937), human epithelial (HeLa), mouse neuroblastoma x rat glioma hybrid (NG108-15) and rat phaeochromocytoma (PC12) cells. In those cells exhibiting AVD, facilitation of RVD is always observed. Both AVD induction and RVD facilitation as well as succeeding apoptotic events can be abolished by prior treatment with a blocker of volume-regulatory K+ or Cl- channels, suggesting that AVD is caused by normotonic activation of ion channels that are normally involved in RVD under hypotonic conditions. Therefore, it is likely that G protein-coupled receptors involved in RVD regulation and death receptors triggering AVD may share common downstream signals which should give us key clues to the detailed mechanisms of volume regulation and survival of animal cells. In this Topical Review, we look at the physiological ionic mechanisms of cell volume regulation and cell death-associated volume changes from the facet of receptor-mediated cellular processes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Channels (Austin)
                Journal ID (iso-abbrev): Channels (Austin)
                Journal ID (publisher-id): KCHL
                Journal ID (publisher-id): kchl20
                Title: Channels
                Publisher: Taylor & Francis
                ISSN (Print): 1933-6950
                ISSN (Electronic): 1933-6969
                Publication date Collection: 2017
                Publication date (Electronic): 31 August 2016
                Publication date PMC-release: 31 August 2016
                Volume: 11
                Issue: 2
                Pages: 167-172
                Affiliations
                [a ]Japan Society for the Promotion of Science , Chiyoda-ku, Japan
                [b ]Department of Cell Physiology, National Institute for Physiological Sciences, National Institutes of Natural Sciences , Okazaki, Japan
                [c ]Department of Physiology, School of Medicine, Fukuoka University , Fukuoka, Japan
                [d ]International Collaborative Research Project, National Institute for Physiological Sciences , Okazaki, Japan
                [e ]SOKENDAI (The Graduate University for Advanced Studies) , Hayama, Kanagawa, Japan
                Author notes
                CONTACT Yasunobu Okada okada@ 123456soken.ac.jp SOKENDAI (The Graduate University for Advanced Studies) , Shonan Village, Hayama, Kanagawa 240-0193, Japan
                Article
                Publisher ID: 1230574
                DOI: 10.1080/19336950.2016.1230574
                PMC ID: 5398604
                PubMed ID: 27579940
                SO-VID: 4337489e-3474-4230-b1ad-96cfc6b52b9d
                Copyright © © 2017 The Author(s). Published with license by Taylor & Francis
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.

                History
                Date received : 17 August 2016
                Date accepted : 25 August 2016
                Related
                Addendum to: Sato-Numata K, et al. Distinct pharmacological and molecular properties of the acid-sensitive outwardly rectifying (ASOR) anion channel from those of the volume-sensitive outwardly rectifying (VSOR) anion channel. Pflügers Arch Eur J Physiol 2016; 468: 795-803; http://dx.doi.org/[ Cross Ref]
                Page count
                Figures: 3, Tables: 0, References: 21, Pages: 6
                Categories
                Subject: Article Addendum

                ScienceOpen disciplines: Molecular biology
                Keywords: activation,anion channel,asor,inactivation,lrrc8,vrac,vsor
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: activation, anion channel, asor, inactivation, lrrc8, vrac, vsor

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