Membrane chloride conductance and capacitance in Jurkat T lymphocytes during osmotic swelling

Ross, Paul; Garber, Sarah S.; Cahalan, Michael D.

doi:10.1016/s0006-3495(94)80754-4

Cited by 87 publications

(72 citation statements)

References 50 publications

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“…This has also been observed by other investigators, but the mechanisms remain unclear (Ross et al, 1994). Cells recorded in isosmotic solutions remained stable or decreased in volume a small amount (−7.7 ± 6.9%) (n = 4).…”

Section: Osmotically Activated CL Currents Correlate With Cell Swellingsupporting

confidence: 84%

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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Section: Osmotically Activated CL Currents Correlate With Cell Swellingsupporting

confidence: 84%

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

Chien¹,

Hartzell²

2007

J Cell Biol

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“…2 to 4), is an intrinsic property of animal cells (24). Through the use of various techniques and cell types, it has been estimated that 40 to 1,000% excess membrane is stored in membrane folds, microvilli, and caveolae (17,19,52,55,61,72,73). Many mechanisms could contribute to such complexity in the 3D organization of the plasma membrane; these include lipid compositions (8,29), membrane-protein interactions (20,44), and cytoskeletal elements (spectrin-ankyrin network, F-actin, microtubules, intermediate filaments, and so forth) (24,31).…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylinositol-4,5-Bisphosphate-Rich Plasma Membrane Patches Organize Active Zones of Endocytosis and Ruffling in Cultured Adipocytes

Huang

Lifshitz

Patki-Kamath

et al. 2004

Molecular and Cellular Biology

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A major regulator of endocytosis and cortical F-actin is thought to be phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P 2 ] present in plasma membranes. Here we report that in 3T3-L1 adipocytes, clathrin-coated membrane retrieval and dense concentrations of polymerized actin occur in restricted zones of high endocytic activity. Ultrafast-acquisition and superresolution deconvolution microscopy of cultured adipocytes expressing an enhanced green fluorescent protein-or enhanced cyan fluorescent protein (ECFP)-tagged phospholipase C␦1 (PLC␦1) pleckstrin homology (PH) domain reveals that these zones spatially coincide with large-scale PtdIns(4,5)P 2 -rich plasma membrane patches (PRMPs). PRMPs exhibit lateral dimensions exceeding several micrometers, are relatively stationary, and display extensive local membrane folding that concentrates PtdIns(4,5)P 2 in three-dimensional space. In addition, a higher concentration of PtdIns(4,5)P 2 in the membranes of PRMPs than in other regions of the plasma membrane can be detected by quantitative fluorescence microscopy. Vesicular structures containing both clathrin heavy chains and PtdIns(4,5)P 2 are revealed immediately beneath PRMPs, as is dense F actin. Blockade of PtdIns(4,5)P 2 function in PRMPs by high expression of the ECFP-tagged PLC␦1 PH domain inhibits transferrin endocytosis and reduces the abundance of cortical F-actin. Membrane ruffles induced by the expression of unconventional myosin 1c were also found to localize at PRMPs. These results are consistent with the hypothesis that PRMPs organize active PtdIns(4,5)P 2 signaling zones in the adipocyte plasma membrane that in turn control regulators of endocytosis, actin dynamics, and membrane ruffling.Phosphatidylinositol-4,5-bisphosphate [PtdIns(4,5)P 2 ] constitutes only about 1% of the total phospholipid in the plasma membrane but plays major roles in regulating multiple cellular processes. Classically, PtdIns(4,5)P 2 was established as the precursor of two intracellular second messengers, inositol-1,4,5-trisphosphate [Ins(3,4,5)P 3 ] and diacylglycerol, generated through the regulation of phospholipase C (PLC) (57). The subsequent discovery of phosphoinositide 3-kinases (9) revealed that PtdIns(4,5)P 2 was also the substrate for the synthesis of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P 3 ], an important second messenger involved in insulin and growth factor signaling, cytoskeletal remodeling, and cell proliferation and survival (63, 65). More recently, it was shown that PtdIns(4,5)P 2 itself functions to regulate the actin cytoskeleton, membrane trafficking, and plasma membrane ion channels and transporters (14,15,24,25,54,58,62). Consequently, this extraordinary versatility of PtdIns(4,5)P 2 in cellular signaling led to the suggestion that there are spatially and functionally segregated pools of PtdIns(4,5)P 2 in the plasma membrane (32,43,44,48). Furthermore, unlike conventional signaling molecules [e.g., Ca 2ϩ , Ins(3,4,5)P 3 , and PtdIns(3,4,5)P 3 ] that, upon receptor activation, show drama...

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“…In other cell systems, a primary role exists for volumeactivated outwardly rectifying Cl Ϫ channels in cell volume regulation (6,(22)(23)(24)36,(55)(56)(57)(58)(59). Thus, in response to swelling, Cl Ϫ channels mediate the net efflux of anions, which in turn promotes an RVD (60 -62).…”

Section: Discussionmentioning

confidence: 99%

Chloride Channels Regulate HIT Cell Volume but Cannot Fully Account for Swelling-Induced Insulin Secretion

Kinard¹,

Goforth²,

Qing³

et al. 2001

Diabetes

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Insulin-secreting pancreatic islet ␤-cells possess anionpermeable Cl؊ channels (I Cl,islet ) that are swelling-activated, but the role of these channels in the cells is unclear. The Cl ؊ channel blockers 4,4-diisothiocyanostilbene-2,2-disulfonic acid (DIDS) and niflumic acid were evaluated for their ability to inhibit I Cl,islet in clonal ␤-cells (HIT cells). Both drugs blocked the channel, but the blockade due to niflumic acid was less voltage-dependent than the blockade due to DIDS. HIT cell volume initially increased in hypotonic solution and was followed by a regulatory volume decrease (RVD). The addition of niflumic acid and, to a lesser extent, DIDS to the hypotonic solution potentiated swelling and blocked the RVD. In isotonic solution, niflumic acid produced swelling, suggesting that islet Cl ؊ channels are activated under basal conditions. The channel blockers glyburide, gadolinium, or tetraethylammonium-Cl did not alter hypotonic-induced swelling or volume regulation. The Na/K/2Cl transport blocker furosemide produced cell shrinkage in isotonic solution and blocked cell swelling normally induced by hypotonic solution. Perifused HIT cells secreted insulin when challenged with hypotonic solutions. However, this could not be completely attributed to I Cl,islet -mediated depolarization, because secretion persisted even when Cl ؊ channels were fully blocked. To test whether blocker-resistant secretion occurred via a distal pathway, distal secretion was isolated using 50 mmol/l potassium and diazoxide. Under these conditions, glucose-dependent secretion was blunted, but hypotonically induced secretion persisted, even with Cl ؊ channel blockers present. These results suggest that ␤-cell swelling stimulates insulin secretion primarily via a distal I Cl,isletindependent mechanism, as has been proposed for K ATPindependent glucose-and sulfonylurea-stimulated insulin secretion. Reverse transcriptase-polymerase chain reaction of HIT cell mRNA identified a CLC-3 transcript in HIT cells. In other systems, CLC-3 is believed to mediate swelling-induced outwardly rectify-

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Membrane chloride conductance and capacitance in Jurkat T lymphocytes during osmotic swelling

Cited by 87 publications

References 50 publications

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

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

Phosphatidylinositol-4,5-Bisphosphate-Rich Plasma Membrane Patches Organize Active Zones of Endocytosis and Ruffling in Cultured Adipocytes

Chloride Channels Regulate HIT Cell Volume but Cannot Fully Account for Swelling-Induced Insulin Secretion

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