Dramatic Magnesium Efflux Induced by High Potassium in Rat Thymocytes

Féray, Jean-Claude; Guerrouache, Karima; Garay, Ricardo P.

doi:10.1006/bbrc.2000.2195

Cited by 3 publications

(2 citation statements)

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“…We realize that this calculation can only be a very rough estimate. In addition, it makes no predictions about the activation mechanism of the Cl Ϫ conductance or whether the change in osmolarity has an additional effect on the K-Cl cotransporter as was described earlier (6). We conclude that human osteoblasts express functional K-Cl cotransporter in their cell membrane.…”

Section: Discussionmentioning

confidence: 56%

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts

Bräuer¹,

Frei²,

Grissmer³

et al. 2003

American Journal of Physiology-Cell Physiology

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The whole cell recording mode of the patch-clamp technique was used to study the effect of hypotonic NaCl or isotonic high-KCl solution on membrane currents in a human osteoblast-like cell line, C1. Both hypotonic NaCl or isotonic high-KCl solution activated Cl- channels expressed in these cells as described previously. The reversal potential of the induced Cl- current is more negative when activated through hypotonic NaCl solution (-47 +/- 5 mV; n = 6) compared with activation through isotonic high-KCl solution (-35 +/- 3 mV; n = 8). This difference can be explained by an increase in intracellular [Cl-] through the activity of a K-Cl cotransporter. Potassium aspartate was unable to activate the current, and furosemide or DIOA suppressed the increase in Cl- current induced by isotonic high-KCl solution. In addition, we used the polymerase chain reaction to demonstrate the presence of KCC1-KCC4 mRNA in the osteoblast-like cell line. From these results, we conclude that human osteoblasts express functional K-Cl cotransporters in their cell membrane that seem to be able to induce the indirect activation of volume-sensitive Cl- channels by KCl through an increase in the intracellular ion concentration followed by water influx and cell swelling.

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Section: Discussionmentioning

confidence: 56%

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts

Bräuer¹,

Frei²,

Grissmer³

et al. 2003

American Journal of Physiology-Cell Physiology

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“…Pharmacological studies of coupled K/Cl fluxes might be biased by the sensitivity of the VSOR Cl − channels to the only available inhibitor of K-Cl cotransport, DIOA. Reported massive DIOA-sensitive Mg 2+ -efflux from thymocytes at high [K + ] [42] could also be affected by the sensitivity of the VSOR Cl − channel to this substance.…”

Section: Discussionmentioning

confidence: 99%

Swelling-Activated Anion Channels Are Essential for Volume Regulation of Mouse Thymocytes

Kurbannazarova

Bessonova

Okada

et al. 2011

IJMS

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Channel-mediated trans-membrane chloride movement is a key process in the active cell volume regulation under osmotic stress in most cells. However, thymocytes were hypothesized to regulate their volume by activating a coupled K-Cl cotransport mechanism. Under the patch-clamp, we found that osmotic swelling activates two types of macroscopic anion conductance with different voltage-dependence and pharmacology. At the single-channel level, we identified two types of events: one corresponded to the maxi-anion channel, and the other one had characteristics of the volume-sensitive outwardly rectifying (VSOR) chloride channel of intermediate conductance. A VSOR inhibitor, phloretin, significantly suppressed both macroscopic VSOR-type conductance and single-channel activity of intermediate amplitude. The maxi-anion channel activity was largely suppressed by Gd3+ ions but not by phloretin. Surprisingly, [(dihydroindenyl)oxy] alkanoic acid (DIOA), a known antagonist of K-Cl cotransporter, was found to significantly suppress the activity of the VSOR-type single-channel events with no effect on the maxi-anion channels at 10 μM. The regulatory volume decrease (RVD) phase of cellular response to hypotonicity was mildly suppressed by Gd3+ ions and was completely abolished by phloretin suggesting a major impact of the VSOR chloride channel and modulatory role of the maxi-anion channel. The inhibitory effect of DIOA was also strong, and, most likely, it occurred via blocking the VSOR Cl− channels.

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Regulation of K-Cl Cotransport: from Function to Genes

2004

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This review intends to summarize the vast literature on K-Cl cotransport (COT) regulation from a functional and genetic viewpoint. Special attention has been given to the signaling pathways involved in the transporter's regulation found in several tissues and cell types, and more specifically, in vascular smooth muscle cells (VSMCs). The number of publications on K-Cl COT has been steadily increasing since its discovery at the beginning of the 1980s, with red blood cells (RBCs) from different species (human, sheep, dog, rabbit, guinea pig, turkey, duck, frog, rat, mouse, fish, and lamprey) being the most studied model. Other tissues/cell types under study are brain, kidney, epithelia, muscle/smooth muscle, tumor cells, heart, liver, insect cells, endothelial cells, bone, platelets, thymocytes and Leishmania donovani. One of the salient properties of K-Cl-COT is its activation by cell swelling and its participation in the recovery of cell volume, a process known as regulatory volume decrease (RVD). Activation by thiol modification with N-ethylmaleimide (NEM) has spawned investigations on the redox dependence of K-Cl COT, and is used as a positive control for the operation of the system in many tissues and cells. The most accepted model of K-Cl COT regulation proposes protein kinases and phosphatases linked in a chain of phosphorylation/dephosphorylation events. More recent studies include regulatory pathways involving the phosphatidyl inositol/protein kinase C (PKC)-mediated pathway for regulation by lithium (Li) in low-K sheep red blood cells (LK SRBCs), and the nitric oxide (NO)/cGMP/protein kinase G (PKG) pathway as well as the platelet-derived growth factor (PDGF)-mediated mechanism in VSMCs. Studies on VSM transfected cells containing the PKG catalytic domain demonstrated the participation of this enzyme in K-Cl COT regulation. Commonly used vasodilators activate K-Cl COT in a dose-dependent manner through the NO/cGMP/PKG pathway. Interaction between the cotransporter and the cytoskeleton appears to depend on the cellular origin and experimental conditions. Pathophysiologically, K-Cl COT is altered in sickle cell anemia and neuropathies, and it has also been proposed to play a role in blood pressure control. Four closely related human genes code for KCCs (KCC1-4). Although considerable information is accumulating on tissue distribution, function and pathologies associated with the different isoforms, little is known about the genetic regulation of the KCC genes in terms of transcriptional and post-transcriptional regulation. A few reports indicate that the NO/cGMP/PKG signaling pathway regulates KCC1 and KCC3 mRNA expression in VSMCs at the post-transcriptional level. However, the detailed mechanisms of post-transcriptional regulation of KCC genes and of regulation of KCC2 and KCC4 mRNA expression are unknown. The K-Cl COT field is expected to expand further over the next decades, as new isoforms and/or regulatory pathways are discovered and its implication in health and disease is revealed.

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Dramatic Magnesium Efflux Induced by High Potassium in Rat Thymocytes

Cited by 3 publications

References 4 publications

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts

Swelling-Activated Anion Channels Are Essential for Volume Regulation of Mouse Thymocytes

Regulation of K-Cl Cotransport: from Function to Genes

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Dramatic Magnesium Efflux Induced by High Potassium in Rat Thymocytes

Cited by 3 publications

References 4 publications

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl– channels in human osteoblasts

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl– channels in human osteoblasts

Swelling-Activated Anion Channels Are Essential for Volume Regulation of Mouse Thymocytes

Regulation of K-Cl Cotransport: from Function to Genes

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Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts

Influence of K-Cl cotransporter activity on activation of volume-sensitive Cl^– channels in human osteoblasts