Opsonized zymosan-stimulated granulocytes-activation and activity of the superoxide-generating system and membrane potential changes

Cohen, HJ; Newburger, PE; Chovaniec, Margaret E.; Whitin, JC; Simons, ER

doi:10.1182/blood.v58.5.975.bloodjournal585975

Cited by 11 publications

(19 citation statements)

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“…Cells were pelleted onto glass slides with a cytocentrifuge, fixed for 2 minutes in methanol, and counterstained with safrinin for 2 minutes. At least 200 cells/sample were scored for the presence of purple black formazan precipitate (Cohen et al, 1981).…”

Section: Hl-60 Cell Maturationmentioning

confidence: 99%

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Brennan

Lee

Abboud

et al. 1987

Journal Cellular Physiology

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We have studied the interactions of dimethyl sulfoxide (DMSO), Giant Cell Tumor (GCT) cell-conditioned medium (GCT CM), and highly purified granulocyte-macrophage colony-stimulating factors (GM-CSF) on the growth and maturation of a highly passaged population of HL-60 cells. DMSO produced dose-dependent inhibition of HL-60 growth in liquid and semisolid media. Growth was partially to completely restored by the addition of GCT CM to cultures. Experiments in which cell volume, cell cycle kinetics, tritiated thymidine (3HTdr) incorporation, cell number, and nitroblue tetrazolium (NBT) reduction were compared during culture indicated that DMSO inhibited the spontaneous increase in cell volume and flow of cells through the cell cycle which occurred in the first day of culture, the increase in 3HTdr incorporation which was detectable by day 2; and the increment in cell counts which occurred by day 3. These effects were opposed by GCT CM. In contrast, the DMSO-induced increase in NBT reduction which occurred by day 6 was not influenced by GCT CM. The major principle opposing DMSO was GM-CSF, since (1) highly purified GM-CSF from GCT cells and recombinant GM-CSF from COS cells transfected with the Mo cell GM-CSF gene overcame greater than 50% of DMSO inhibition; and (2) conditioned media from cells not producing CSF, G-CSF from GCT cells, and recombinant G-CSF from Escherichia coli transfected with the G-CSF gene from 5,637 cells were inactive. DMSO had little or no effect on the elaboration of autostimulatory activity by HL-60 cells. DMSO is a useful agent for inhibiting the spontaneous growth of HL-60 cells and restoring their dependence on GM-CSF, a property which may be mediated through the effects of DMSO on cell cycle kinetics and/or maturation.

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Section: Hl-60 Cell Maturationmentioning

confidence: 99%

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Brennan

Lee

Abboud

et al. 1987

Journal Cellular Physiology

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“…Dependence of PMNL membrane depolarization on extracellular Na+ and K+ It has previously been demonstrated that the relative changes in diSC3-6) fluorescence upon cell stimulation can be used to measure changes in the transmembrane potential of human platelets (Horne and Simons, 1978;Greenberg-Sepersky and Simons, 1984;Greenberg-Sepersky and Simons, 1985) and PMNL (Seligman et al, 1980;Whitin et al, 1980;Cohen et al, 1981;Jones et al, 1981;Simchowitz et al, 1982). In parallel with platelets, for which the rate of stimulus-induced efflux of diSC3-(Ei) is a more consistent measure of the response than the overall relative extent of the change (Greenberg-Sepersky and Simons, 19841, the PMNL response can be quantitated in terms of the rate of fluorescence change.…”

Section: Resultsmentioning

confidence: 99%

“…Our studies aim to clarify the role of Na+ and K + transmembrane gradients in the immune complex-stimulated transmembrane potential change and the activation of the respiratory burst of human PMNL prepared by water or NH&1 lysis techniques. 01988 ALAN R. LISS, INC. It has been demonstrated that a change in the resting membrane potential, detectable within seconds after stimulus addition and dependent upon the Na+/K+ transmembrane gradients, occurs with virtually all stimuli but is not necessary for cell stimulation (Korchak and Weissman, 1978;Whitin et al, 1980;Seligman et al, 1980;Cohen et al, 1981) since unopsonized Candida albicans hyphae bypass this step (Lyman et al, 1987). Recent studies have documented a rapid release of intracellular stores of calcium ions accompanying PMNL activation (White et al, 1983;Korchak et al, 1984;Apfeldorf et al, 1985;Lazzari et al, 1986) by several stimuli but not by phorbol myristate 13-acetate (PMA) (Lehrmeyer et al, 1979).…”

mentioning

confidence: 99%

The role of transmembrane cationic gradients in immune complex stimulation of human polymorphonuclear leukocytes

Luscinskas

Mark

Brunkhorst

et al. 1988

Journal Cellular Physiology

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The role of monovalent cationic gradients in human polymorphonuclear leukocyte (PMNL) stimulation was investigated by monitoring immune complex-stimulated transmembrane depolarization and superoxide production, events which accompany--and have been used as indicators of --PMNL activation. Abolishing only the Na+ gradient by substitution of choline for extracellular Na+ did not affect the resting membrane potential but reduced the rate of stimulus-induced transmembrane depolarization to 50% of control. In contrast, collapsing both Na+ and K+ gradients by suspension in K+ buffer (high K-PRK) depolarized the cells and reduced the stimulus-induced rate of depolarization to 11% of control. Pretreatment of cells suspended in Na+ buffers with 5-(N,N-dimethyl)amiloride hydrochloride (DMA) or with valinomycin reduced by one-half the rate of immune complex induced membrane depolarization. Conversely, in the absence of either or of both Na+ or K+ gradients, or in the presence of valinomycin, immune complex elicited an enhanced rate of superoxide production. However, PMNL prepared via NH4Cl (NH4Cl-PMNL) instead of H2O (H2O-PMNL) lysis of residual red blood cells exhibited an absolute requirement for an intact Na+ gradient in cell stimulation. The present results thus demonstrate that: 1) both Na+ and K+ gradients participate equally in the membrane depolarization elicited by immune complex; 2) neither a Na+ or a K+ gradient is required for immune complex activation, or for activity of the respiratory burst; and 3) an artifactual requirement for an intact Na+ gradient occurs in neutrophils prepared by the NH4Cl lysis technique.

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“…This represents <0.01% of the 3 9 10 10 electrons translocated by a human eosinophil during the respiratory burst (42). One consequence is that a number of careful studies published between 1978 and 1983 concluded that membrane depolarization was the trigger for the respiratory burst because measurable depolarization preceded detectable superoxide production (145)(146)(147)(148)(149)(150)(151). Of course, thanks to the incisive studies of Henderson, Chappell, and colleagues (1-3), we now know that the opposite is the casedepolarization is a direct consequence of the electrogenic activity of NADPH oxidase.…”

Section: The Scale Of the Phagocyte Respiratory Burstmentioning

confidence: 99%

The intimate and controversial relationship between voltage‐gated proton channels and the phagocyte NADPH oxidase

DeCoursey

2016

Immunological Reviews

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Summary One of the most fascinating and exciting periods in my scientific career entailed dissecting the symbiotic relationship between two membrane transporters, the NADPH oxidase complex and voltage gated proton channels (HV1). By the time I entered this field, there had already been substantial progress toward understanding NADPH oxidase, but HV1 were known only to a tiny handful of cognoscenti around the world. Having identified the first proton currents in mammalian cells in 1991, I needed to find a clear function for these molecules if the work was to become fundable. The then-recent discoveries of Henderson, Chappell, and colleagues in 1987–1988 that led them to hypothesize interactions of both molecules during the respiratory burst of phagocytes provided an excellent opportunity. In a nutshell, both transporters function by moving electrical charge across the membrane: NADPH oxidase moves electrons and HV1 moves protons. The consequences of electrogenic NADPH oxidase activity on both membrane potential and pH strongly self-limit this enzyme. Fortunately, both consequences specifically activate HV1, and HV1 activity counteracts both consequences, a kind of yin-yang relationship. Notwithstanding a decade starting in 1995 when many believed the opposite, these are two separate molecules that function independently despite their being functionally interdependent in phagocytes. The relationship between NADPH oxidase and HV1 has become a paradigm that somewhat surprisingly has now extended well beyond the phagocyte NADPH oxidase -- an industrial strength producer of reactive oxygen species (ROS) -- to myriad other cells that produce orders of magnitude less ROS for signaling purposes. These cells with their seven NADPH oxidase (NOX) isoforms provide a vast realm of mechanistic obscurity that will occupy future studies for years to come.

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Opsonized zymosan-stimulated granulocytes-activation and activity of the superoxide-generating system and membrane potential changes

Cited by 11 publications

References 0 publications

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

Interactions of dimethyl sulfoxide and granulocyte‐macrophage colony‐stimulating factors on the growth and maturation of HL‐60 cells

The role of transmembrane cationic gradients in immune complex stimulation of human polymorphonuclear leukocytes

The intimate and controversial relationship between voltage‐gated proton channels and the phagocyte NADPH oxidase

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