Regulation of eosinophil membrane depolarization during NADPH oxidase activation

Bankers-Fulbright, Jennifer L.; Gleich, Gerald J.; Kephart, Gail M.; Kita, Hirohito; O’Grady, Scott M.

doi:10.1242/jcs.00627

Cited by 33 publications

(42 citation statements)

References 33 publications

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“…We showed that the characteristic V m depolarization in the bud at 6 hpa mechanistically mimics the well-known NADPH oxidasedriven depolarization in immune cells during an oxidative burst (Bankers-Fulbright et al, 2003). This makes it attractive to speculate that V m depolarization is a by-product of ROS production, which is reinforced by the non-requirement of V m depolarization for regeneration.…”

Section: Homeostatic (From 48 Hpa)mentioning

confidence: 54%

Early bioelectric activities mediate redox-modulated regeneration

et al. 2016

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Reactive oxygen species (ROS) and electric currents modulate regeneration; however, the interplay between biochemical and biophysical signals during regeneration remains poorly understood. We investigate the interactions between redox and bioelectric activities during tail regeneration in Xenopus laevis tadpoles. We show that inhibition of NADPH oxidase-mediated production of ROS, or scavenging or blocking their diffusion into cells, impairs regeneration and consistently regulates the dynamics of membrane potential, transepithelial potential (TEP) and electric current densities (J I ) during regeneration. Depletion of ROS mimics the altered TEP and J I observed in the non-regenerative refractory period. Short-term application of hydrogen peroxide (H 2 O 2 ) rescues (from depleted ROS) and induces (from the refractory period) regeneration, TEP increase and J I reversal. H 2 O 2 is therefore necessary for and sufficient to induce regeneration and to regulate TEP and J I . Epistasis assays show that voltage-gated Na + channels act downstream of H 2 O 2 to modulate regeneration. Altogether, these results suggest a novel mechanism for regeneration via redoxbioelectric orchestration.

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Section: Homeostatic (From 48 Hpa)mentioning

confidence: 54%

Early bioelectric activities mediate redox-modulated regeneration

et al. 2016

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“…The extrusion of electrons across the membrane to generate superoxide develops a potential across the membrane. The depolarization will impose bioenergetic limits on the enzyme activity and thus curtail ROS generation if there is no route for charge compensation (Henderson et al, 1987;Bankers-Fulbright et al, 2003;Rada et al, 2005). Although several ion channels have been ascribed this role in other cell types, an issue that has proven highly controversial (DeCoursey, 2003;Ahluwalia et al, 2004), it is evident that any functional conductance in the membrane during NOX2 activity will inevitably contribute to setting the membrane potential.…”

Section: Discussionmentioning

confidence: 99%

“…We therefore propose a novel feedforward mechanism, whereby activation of the oxidase and resultant ROS production promotes a redox-controlled structural transition of CLIC1 and promotes its insertion into the membrane where it carries an anion conductance. The increase in CLIC1-mediated chloride conductance then facilitates ROS generation by NOX2 by providing a conductance that offsets the membrane potential change generated by NOX2 activity and permitting sustained ROS generation by the oxidase (Henderson et al, 1987;Bankers-Fulbright et al, 2003;Rada et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

CLIC1 Function Is Required for β-Amyloid-Induced Generation of Reactive Oxygen Species by Microglia

Milton¹,

Abeti²,

Averaimo³

et al. 2008

J. Neurosci.

129

131

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The Alzheimer's disease (AD) brain is characterized by plaques containing ␤-amyloid (A␤) protein surrounded by astrocytes and reactive microglia. Activation of microglia by A␤ initiates production of reactive oxygen species (ROS) by the plasmalemmal NADPH oxidase; the resultant oxidative stress is thought to contribute to neurodegeneration in AD. We have previously shown that A␤ upregulates a chloride current mediated by the chloride intracellular channel 1 (CLIC1) protein in microglia. We now demonstrate that A␤ promotes the acute translocation of CLIC1 from the cytosol to the plasma membrane of microglia, where it mediates a chloride conductance. Both the A␤ induced Cl Ϫ conductance and ROS generation were prevented by pharmacological inhibition of CLIC1, by replacement of chloride with impermeant anions, by an anti-CLIC1 antibody and by suppression of CLIC1 expression using siRNA. Thus, the CLIC1-mediated Cl Ϫ conductance is required for A␤-induced generation of neurotoxic ROS by microglia. Remarkably, CLIC1 activation is itself dependent on oxidation by ROS derived from the activated NADPH oxidase. We therefore propose that CLIC1 translocation from the cytosol to the plasma membrane, in response to redox modulation by NADPH oxidase-derived ROS, provides a feedforward mechanism that facilitates sustained microglial ROS generation by the NAPDH oxidase.

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“…This electron movement can be recorded directly as an electrical current (10,5). Because the electron transport is not obligatorily coupled to a compensatory charge movement, it produces a separation of charge that leads to sustained depolarization of the membrane (62) well beyond 0 mV in intact granulocytes (63)(64)(65)(66). If this charge movement is not compensated, extreme depolarization results (67,61) that by itself directly opposes electron flux across the membrane (25).…”

Section: Introductionmentioning

confidence: 99%

Analysis of Electrophysiological Properties and Responses of Neutrophils

Morgan

DeCoursey

2007

Neutrophil Methods and Protocols

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SummaryThe past decade has seen increasing use of the patch clamp technique on neutrophils and eosinophils. The main goal of these electrophysiological studies has been to elucidate the mechanisms underlying the phagocyte respiratory burst. NADPH oxidase activity, which defines the respiratory burst in granulocytes, is electrogenic because electrons from NADPH are transported across the cell membrane, where they reduce oxygen to form superoxide anion (O 2 − ). This passage of electrons comprises an electrical current that would rapidly depolarize the membrane if the charge movement were not balanced by proton efflux. The patch clamp technique enables simultaneous recording of NADPH oxidase-generated electron current and H + flux through the closely related H + channel. Increasing evidence suggests that other ion channels may play crucial roles in degranulation, phagocytosis, and chemotaxis, highlighting the importance of electrophysiological studies to advance knowledge of granulocyte function. Several configurations of the patch clamp technique exist. Each has advantages and limitations that are discussed here. Meaningful measurements of ion channels cannot be achieved without an understanding of their fundamental properties. We describe the types of measurements that are necessary to characterize a particular ion channel.

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Regulation of eosinophil membrane depolarization during NADPH oxidase activation

Cited by 33 publications

References 33 publications

Early bioelectric activities mediate redox-modulated regeneration

Early bioelectric activities mediate redox-modulated regeneration

CLIC1 Function Is Required for β-Amyloid-Induced Generation of Reactive Oxygen Species by Microglia

Analysis of Electrophysiological Properties and Responses of Neutrophils

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