Calcium/calmodulin-modulated chloride and taurine conductances in cultured rat astrocytes

Li, Guangze; Liu, Yin; Olson, James E.

doi:10.1016/s0006-8993(01)03235-8

Cited by 34 publications

(28 citation statements)

References 58 publications

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“…Taken together, these results indicate not only that the release of taurine does not involve VRAC in intestine 407 cells but also that distinct signaling pathways are involved in the regulation of Cl Ϫ and taurine efflux (54). An increase in intracellular free Ca 2ϩ has been reported to be involved in the activation of taurine efflux for several cell types, including erythroleukemia cells (21), cultured rat astrocytes (33), and rat cerebral cortex (30). In astrocytes and cerebral granule cells, however, the hypotonicity-provoked taurine efflux was independent of [Ca 2ϩ ] i or required basal Ca 2ϩ levels (36,38,40 ] i is required, as observed previously for astrocytes (36).…”

Section: Discussionmentioning

confidence: 79%

Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells

Tomassen¹,

Fekkes²,

Jonge³

et al. 2004

American Journal of Physiology-Cell Physiology

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Human Intestine 407 cells respond to osmotic cell swelling by the activation of Cl−- and K+-selective ionic channels, as well as by stimulating an organic osmolyte release pathway readily permeable to taurine and phosphocholine. Unlike the activation of volume-regulated anion channels (VRAC), activation of the organic osmolyte release pathway shows a lag time of ∼30–60 s, and its activity persists for at least 8–12 min. In contrast to VRAC activation, stimulation of organic osmolyte release did not require protein tyrosine phosphorylation, active p21rho, or phosphatidylinositol 3-kinase activity and was insensitive to Cl− channel blockers. Treatment of the cells with putative organic anion transporter inhibitors reduced the release of taurine only partially or was found to be ineffective. The efflux was blocked by a subclass of organic cation transporter (OCT) inhibitors (cyanine-863 and decynium-22) but not by other OCT inhibitors (cimetidine, quinine, and verapamil). Brief treatment of the cells with phorbol esters potentiated the cell swelling-induced taurine efflux, whereas addition of the protein kinase C (PKC) inhibitor GF109203X largely inhibited the response, suggesting that PKC is involved. Increasing the level of intracellular Ca2+ by using A-23187- or Ca2+-mobilizing hormones, however, did not affect the magnitude of the response. Taken together, the results indicate that the hypotonicity-induced efflux of organic osmolytes is independent of VRAC and involves a PKC-dependent step.

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Section: Discussionmentioning

confidence: 79%

Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells

Tomassen¹,

Fekkes²,

Jonge³

et al. 2004

American Journal of Physiology-Cell Physiology

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“…This process, termed regulatory volume decrease (RVD), is mediated in part by activation of membrane channels that are capable of conducting small organic molecules such as amino acids (Olson and Li, 1997). We have described a cell volume-activated and calcium-dependent anion cur-rent in cultured rat astrocytes that is capable of conducting anionic taurine (Li et al, 2002) and appears similar to volume-dependent anion and amino acid channels described in other cell types (Jackson and Strange, 1993;Jalonen, 1993;Roy and Banderali, 1994).…”

Section: Introductionmentioning

confidence: 81%

“…Modification of intracellular calcium levels and activation of various kinases have been related to cell swelling, RVD, osmolyte fluxes, and membrane channel activities (Worrell and Frizzell, 1991;Bender et al, 1993;Crepel et al, 1998;Estevez et al, 2001;Xu et al, 2001;Li et al, 2002). In rat cerebral astrocytes, we have described the dependence on extracellular calcium, L-type calcium channels, and calmodulin activity of cell swelling-induced activation of chloride and taurine conductances (Li et al, 2002). The role of intracellular calcium and calmodulin in this response to swelling was deduced primarily from pharmacological manipulations.…”

Section: Introductionmentioning

confidence: 99%

Volume‐regulated anion conductance in cultured rat cerebral astrocytes requires calmodulin activity

Olson

2004

Glia

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We examined the calmodulin dependence of anion channel activation during hypo-osmotic swelling in rat cerebral astrocytes. Control cells bathed in iso-osmotic (290 mOsm) phosphate-buffered saline (PBS) and recorded using a patch electrode containing 140 mM KCl increased membrane conductance threefold over basal levels after 12 min in hypo-osmotic (200 mOsm) PBS. Cells injected with monoclonal anticalmodulin antibody demonstrated no increase in membrane conductance during a subsequent exposure to hypo-osmotic PBS. In contrast, cells iontophoretically injected with monoclonal antiglial fibrillary acidic protein antibody or with anticalmodulin antibody absorbed with an excess of free calmodulin demonstrated an increase in conductance during hypo-osmotic exposure similar to that of control cells. Conductance in iso-osmotic conditions was unchanged by antibody injection. Similar results were obtained when using patch electrode and bath solutions containing chloride as the only cell permeant ion, indicating a calmodulin-dependent anion current is activated with this degree of hypo-osmotic treatment. Western blots confirmed the specificity of the anticalmodulin and antiglial fibrillary acidic protein antibodies used in this study for proteins of 17 and 51 kD, respectively. In addition, in vitro studies demonstrated inhibition of the calmodulin-dependent activation of phosphodiesterase by the anticalmodulin antibody. Thus, binding of this antibody to calmodulin causes functional inhibition of calmodulin activity. No change in the intensity or cellular distribution of calmodulin immunostaining was observed during 30 min of hypo-osmotic exposure. However, increased immunostaining for activated calmodulin kinase IIalpha was observed after 10 min of hypo-osmotic exposure, suggesting initiation of calmodulin-dependent processes by cell swelling. The data indicate calmodulin activity is critical for activation of volume-regulated anion channels in rat cerebral astrocytes.

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“…VB). Addition of Ca 2ϩ -mobilizing agonists does not elicit taurine release under isotonic conditions but potentiates the swelling-induced taurine efflux from a variety of cells presumably via pathways involving CaM and CaMKII, PI3K, and PKC (112,222,451,551,661). In contrast, a concentration (3 nM) of LTD 4 too low to elicit detectable Ca 2ϩ mobilization induces taurine release under isotonic conditions (see Fig.…”

Section: Mechanisms Of Activation Of the Taurine Efflux Pathwaymentioning

confidence: 90%

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,243

1,626

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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, Ca2+, 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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Calcium/calmodulin-modulated chloride and taurine conductances in cultured rat astrocytes

Cited by 34 publications

References 58 publications

Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells

Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells

Volume‐regulated anion conductance in cultured rat cerebral astrocytes requires calmodulin activity

Physiology of Cell Volume Regulation in Vertebrates

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