Mitogen induction of ion channels in murine T lymphocytes.

DeCoursey, Thomas E.; Chandy, K. George; Gupta, Sudhir; Cahalan, Michael D.

doi:10.1085/jgp.89.3.405

Cited by 114 publications

(64 citation statements)

References 21 publications

(43 reference statements)

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“…In G2/M the cell membrane becomes depolarized and K ϩ flux is decreased, with a corresponding increase in Cl channel conductance (9). In addition to the long recognized role of ion channels in cellular proliferation, the reverse is also true, as mitogens have been shown to up-regulate potassium channels including Kv1.3 (10,11).…”

Section: The Maintenance Of T Cell Memory Is Critical For the Developmentioning

confidence: 99%

Functional Blockade of the Voltage-gated Potassium Channel Kv1.3 Mediates Reversion of T Effector to Central Memory Lymphocytes through SMAD3/p21cip1 Signaling

Gocke

Knapp

et al. 2012

Journal of Biological Chemistry

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Background:The role of Kv1.3 in regulating T cell differentiation and memory is incompletely understood. Results: A dominant negative mutation of Kv1.3 mediates reversion of T EM into T CM through SMAD3-dependent cell cycle changes. Conclusion: Signaling through Kv1.3 is a mechanism by which T EM may revert to T CM . Significance: These findings suggest a novel role for Kv1.3 in T cell differentiation and memory responses.

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Section: The Maintenance Of T Cell Memory Is Critical For the Developmentioning

confidence: 99%

Functional Blockade of the Voltage-gated Potassium Channel Kv1.3 Mediates Reversion of T Effector to Central Memory Lymphocytes through SMAD3/p21cip1 Signaling

Gocke

Knapp

et al. 2012

Journal of Biological Chemistry

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“…Deutsch and colleagues found an increase in gK~v) of 1.7-fold for 1-and 2-d PHA-activated T ceils after mitogenic activation (Deutsch, Krause, and Lee, 1986). In mouse T cells, a relatively larger increase in the number of K(V) channels after mitogenic activation represents an increase in the density of K(V) channels; the number of these channels in resting murine T cells is lower than in resting human T cells (DeCoursey, Chandy, Gupta, and Cahalan, 1987b).…”

Section: Changes In Channel Expression That Precede Cell Divisionmentioning

confidence: 99%

Calcium-activated potassium channels in resting and activated human T lymphocytes. Expression levels, calcium dependence, ion selectivity, and pharmacology.

Grissmer

Nguyen

Cahalan

1993

The Journal of General Physiology

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206

143

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Ca2+-activated K+[K(Ca)] channels in resting and activated human peripheral blood T lymphocytes were characterized using simultaneous patch-clamp recording and fura-2 monitoring of cytosolic Ca 2+ concentration, [Ca2+]i . Whole-cell experiments, using EGTA-buffered pipette solutions to raise [CaZ÷]i to 1 p,M, revealed a 25-fold increase in the number of conducting K(Ca) channels per cell, from an average of 20 in resting T cells to > 500 channels per cell in T cell blasts after mitogenic activation. The opening of K(Ca) channels in both whole-cell and inside-out patch experiments was highly sensitive to [Ca2+]i (Hill coefficient of 4, with a midpoint of ~ 300 nM). At optimal [Ca2+]i, the open probability of a K(Ca) channel was 0.3-0.5. K(Ca) channels showed little or no voltage dependence from -100 to 0 inV. Single-channel/-V curves were linear with a unitary conductance of 11 pS in normal Ringer and exhibited modest inward rectification with a unitary conductance of ~35 pS in symmetrical 160 mM K ÷. Permeability ratios, relative to K +, determined from reversal potential measurements were: K + (1.0) > Rb + (0.96) > NH~" (0.17) > Cs ÷ (0.07). Slope conductance ratios were: NH~ (1.2) > K + (1.0) > Rb + (0.6) > Cs ÷ (0.10). Extracellular Cs + or Ba 2+ each induced voltagedependent block of K(Ca) channels, with block increasing at hyperpolarizing potentials in a manner suggesting a site of block 75% across the membrane field from the outside. K(Ca) channels were blocked by tetraethylammonium (TEA) applied externally (Kd = 40 mM), but were unaffected by 10 mM TEA applied inside by pipette perfusion. K(Ca) channels were blocked by charybdotoxin (CTX) with a half-blocking dose of 3-4 nM, but were resistant to block by noxiustoxin (NTX) at 1-100 nM. Unlike K(Ca) channels in Jurkat T cells, the K(Ca) channels of normal resting or activated T cells were not blocked by apamin. We conclude that while K(Ca) and voltage-gated K + channels in the same cells share similarities in ion

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“…The voltage-gated K + channels are widely distributed and involve maintaining electrophysiological stabilization which is essential for salt and water balance in kidney cells (Wang et al, 1992) and guard cells (Schroeder et al, 1994), cell volume regulations (Deutsch and Chen, 1993), electrical excitability in neurons and cardiac muscle (Jan and Jan, 1989), insulin release from pancreatic B-cells (Dukes and Philipson, 1996), activation of T-and Blymphocytes (DeCoursey et al, 1984;Amigorena et al, 1990b), and controlling myeloblastic cell development (Lu et al, 1993). More emerging evidence suggest that K + channels play a crucial role in proliferation control in different cell types including corneal epithelial cells (Decoursey et al, 1987;Freedman et al, 1992;Day et al, 1993;Deutsch and Chen, 1993;Pappone and Ortiz-Miranda, 1993;Xu et al, 1996Xu et al, ,1999Wang et al, 1997;Roderick et al, 2003). The activation of K + channels is involved in the onset of cellular events associated with both T-and B-lymphocyte activation (Amigorena et al, 1990a,b;Lin et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

2006

Progress in Retinal and Eye Research

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One of the functional roles of the corneal epithelial layer is to protect the cornea, lens and other underlying ocular structures from damages caused by environmental insults. It is important for corneal epithelial cells to maintain this function by undergoing continuous renewal through a dynamic process of wound healing. Previous studies in corneal epithelial cells have provided substantial evidence showing that environmental insults, such as ultraviolet (UV) irradiation and other biohazards, can induce stress-related cellular responses resulting in apoptosis and thus interrupt the dynamic process of wound healing. We found that UV irradiation-induced apoptotic effects in corneal epithelial cells are started by the hyperactivation of K + channels in the cell membrane resulting in a fast loss of intracellular K + ions. Recent studies provide further evidence indicating that these complex responses in corneal epithelial cells are resulted from the activation of stressrelated signaling pathways mediated by K + channel activity. The effect of UV irradiation on corneal epithelial cell fate shares common signaling mechanisms involving the activation of intracellular responses that are often activated by the stimulation of various cytokines. One piece of evidence for making this distinction is that at early times UV irradiation activates a Kv3.4 channel in corneal epithelial cells to elicit activation of c-Jun N-terminal kinase cascades and p53 activation leading to cell cycle arrest and apoptosis. The hypothetic model is that UV-induced potassium channel hyperactivity as an early event initiates fast cell shrinkages due to the loss of intracellular potassium, resulting in the activation of scaffolding protein kinases and cytoskeleton reorganizations. This review article presents important control mechanisms that determine Kv channel activity-mediated cellular responses in corneal epithelial cells, involving activation of stress-induced signaling pathways, arrests of cell cycle progression and/or induction of apoptosis.

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Mitogen induction of ion channels in murine T lymphocytes.

Abstract: Using gigohm-seal recording, we studied ion channel expression in resting and activated T lymphocytes from mice . Both the number of channels per cell and the predominant type of K+ channel depend upon the state of activation of the cell . Unstimulated T cells express small numbers of K+

Cited by 114 publications

References 21 publications

Functional Blockade of the Voltage-gated Potassium Channel Kv1.3 Mediates Reversion of T Effector to Central Memory Lymphocytes through SMAD3/p21cip1 Signaling

Functional Blockade of the Voltage-gated Potassium Channel Kv1.3 Mediates Reversion of T Effector to Central Memory Lymphocytes through SMAD3/p21cip1 Signaling

Calcium-activated potassium channels in resting and activated human T lymphocytes. Expression levels, calcium dependence, ion selectivity, and pharmacology.

Stress-induced corneal epithelial apoptosis mediated by K+ channel activation

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