Reactive oxidants regulate membrane repolarization and store-operated uptake of calcium by formyl peptide-activated human neutrophils

Tintinger, Gregory Ronald; Theron, Annette J.; Potjo, Moliehi

doi:10.1016/j.freeradbiomed.2007.03.012

Cited by 15 publications

(12 citation statements)

References 25 publications

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“…In accord with our findings, it has been shown recently that NOX2 regulates neutrophil membrane potential and Ca 2+ influx not only via its electrogenic activity (i.e. catalytic transmembrane electron transfer), but also as a downstream consequence of the generation of ROS [21]. It is well known that Ca 2+ mobilization plays an important role in classical receptor-mediated activation of superoxide production by phagocytic cells [22–24].…”

Section: Discussionsupporting

confidence: 90%

Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca2+/c-Abl signaling pathway

Jamali

Valente

Clark

2010

Free Radical Biology and Medicine

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The importance of H 2 O 2 as a cellular signaling molecule has been demonstrated in a number of cell types and pathways. Here we explore a positive feedback mechanism of H 2 O 2 -mediated regulation of the phagocyte respiratory burst NADPH oxidase (NOX2). H 2 O 2 induced a dose-dependent stimulation of superoxide production in human neutrophils, as well as in K562 leukemia cells overexpressing NOX2 system components. Stimulation was abrogated by addition of catalase, the extracellular Ca 2+ chelator BAPTA, the T-type Ca 2+ channel inhibitor mibefradil, the PKCδ inhibitor rottlerin, or the c-Abl non-receptor tyrosine kinase inhibitor imatinib mesylate, or by over-expression of a dominant-negative form of c-Abl. H 2 O 2 induced phosphorylation of tyrosine 311 on PKCδ and this activating phosphorylation was blocked by treatment with rottlerin, imatinib mesylate, or BAPTA. Rac GTPase activation in response to H 2 O 2 was abrogated by BAPTA, imatinib mesylate, or rottlerin. In conclusion, H 2 O 2 stimulates NOX2-mediated superoxide generation in neutrophils and K562/NOX2 cells via a signaling pathway involving Ca 2+ influx and c-Abl tyrosine kinase acting upstream of PKCδ. This positive feedback regulatory pathway has important implications for amplifying the innate immune response and contributing to oxidative stress in inflammatory disorders.

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Section: Discussionsupporting

confidence: 90%

Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca2+/c-Abl signaling pathway

Jamali

Valente

Clark

2010

Free Radical Biology and Medicine

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“…On the other hand, Ehring et al reported that vanadate compounds act in a similar way as thimerosal: They deplete the ER Ca 2+ stores via thiol oxidation and thus induce activation of I CRAC independently of any kinases or phosphatases [180]. Additional evidence that SOCE is inhibited by oxidizing agents such as homocysteine, H 2 O 2 , HOCl, tBHP and diamide was later provided by several independent groups in different cell types [181][182][183][184]. Particularly interesting are the findings by Redondo et al who observed modest activation of SOCE following treatment with low M concentrations of H 2 O 2 while higher concentrations (low mM) inhibited SOCE in human platelets [185].…”

Section: Reactive Oxygen Species Effects On Soce and Crac/orai Channelsmentioning

confidence: 97%

“…Hawkins et al [188] studied redox mediated activation of STIM1 and found that oxidative stress leads to gluthationylation of STIM1's cysteine 56, triggering STIM1 oligomerization and punctae [171][172][173][174][175][176][177][180][181][182][183][184][185][186]189,[192][193][194][195][203][204][205][206][207][208][209][210][211][212][213][214][215][216][217][218] BSO, buthionine sulfoximine; DEANO, 2-(N,N-diethylamino)diazenolate-2-oxide; FRTL-5, fischer rat thyroid low serum 5%; GEA3162, 1,2,3,4,-oxatriazolium, 5-amino-3-(3,4-dichlorophenyl)-chloride; HEK, human embryonic kidney; IP3R, IP3 receptor; Jurkat, human leukemic T cell line; MEF, mouse embryonic fibroblasts; RBL, rat basophilic leukemia; RyR, ryanodine receptor; SH-SY5Y, human neuroblastoma cell line; SNP, sodium nitroprusside; tBHP, tert-butylhydroperoxide.…”

Section: Reactive Oxygen Species Effects On Soce and Crac/orai Channelsmentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

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a b s t r a c tReactive oxygen species (ROS) are increasingly recognized as second messengers in many cellular processes. While high concentrations of oxidants damage proteins, lipids and DNA, ultimately resulting in cell death, selective and reversible oxidation of key residues in proteins is a physiological mechanism that can transiently alter their activity and function. Defects in ROS producing enzymes cause disturbed immune response and disease.Changes in the intracellular free Ca 2+ concentration are key triggers for diverse cellular functions. Ca 2+ homeostasis thus needs to be precisely tuned by channels, pumps, transporters and cellular buffering systems. Alterations of these key regulatory proteins by reversible or irreversible oxidation alter the physiological outcome following cell stimulation. It is therefore necessary to understand which proteins are regulated and if this regulation is relevant in a physiological-and/or pathophysiological context. Because ROS are inherently difficult to identify and to measure, we first review basic oxygen redox chemistry and methods of ROS detection with special emphasis on electron paramagnetic resonance (EPR) spectroscopy. We then focus on the present knowledge of redox regulation of Ca 2+ permeable ion channels such as voltage-gated (CaV) Ca 2+ channels, transient receptor potential (TRP) channels and Orai channels.© 2011 Elsevier Ltd. All rights reserved. Basic redox chemistry of oxygenMany chemical processes are linked to the exchange of electrons between two or more molecular entities. The transfer of one (or more) electron(s) is associated with oxidation (loss of electron) and reduction (gain of electron) of the components. Such reactions are also known as redox reactions. The processes of reactive oxygen species (ROS) formation and elimination are exclusively of redox nature.Molecular oxygen is the precursor of all ROS. It contains two unpaired electrons in separate (antibonding) orbitals in its outer electron sphere and is thus, by definition, a radical. Radicals have at least one unpaired electron in their orbital system and usually show high reactivity; transition metal ions also may have unpaired electrons, but are not called radicals. Although having radical character, molecular oxygen is chemically rather inert (luckily!), because high * Corresponding authors at: Institut für Biophysik, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: +49 6841 1626453; fax: +49 6841 1626060.E-mail addresses: ivan.bogeski@uks.eu (I. Bogeski), barbara.niemeyer@uks.eu (B.A. Niemeyer).

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“…Membrane depolarization accompanies activation of the phagocyte NADPH oxidase. NADPH oxidase regulates PMN membrane potential and Ca 2+ influx via its electrogenic activity and as a result of generation of ROS (Tintinger et al, 2007). …”

Section: Introductionmentioning

confidence: 99%

Vascular and Cellular Calcium in Normal and Hypertensive Pregnancy

Adamová¹,

Ozkan²,

Khalil³

2009

CCP

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Normal pregnancy is associated with significant hemodynamic changes in the cardiovascular system in order to meet the metabolic demands of mother and fetus. These changes include increased cardiac output, decreased vascular resistance, and vascular remodeling in the uterine and systemic circulation. Preeclampsia (PE) is a major complication of pregnancy characterized by proteinuria and hypertension. Several risk factors have been implicated in the pathogenesis of PE including genetic and dietary factors. Ca 2+ is an essential dietary element and an important regulator of many cellular processes including vascular function. The importance of adequate dietary Ca 2+ intake during pregnancy is supported by many studies. Pregnancy-associated changes in Ca 2+ metabolism and plasma Ca 2+ have been observed. During pregnancy, changes in intracellular free Ca 2+ concentration ([Ca 2+ ] i ) have been described in red blood cells, platelets and immune cells. Also, during pregnancy, an increase in [Ca 2+ ] i in endothelial cells (EC) stimulates the production of vasodilator substances such as nitric oxide and prostacyclin. Normal pregnancy is also associated with decreased vascular smooth muscle (VSM) [Ca 2+ ] i and possibly the Ca 2+ -sensitization pathways of VSM contraction including protein kinase C, Rho-kinase, and mitogen-activated protein kinase. Ca 2+ -dependent matrix metalloproteinases could also promote extracellular matrix degradation and vascular remodeling during pregnancy. Disruption in the balance between dietary, plasma and vascular cell Ca 2+ may be responsible for some of the manifestation of PE including procoagulation, decreased vasodilation, and increased vasoconstriction and vascular resistance. The potential benefits of Ca 2+ supplements during pregnancy, and the use of modulators of vascular Ca 2+ to reduce the manifestations of PE in susceptible women remain an important area for experimental and clinical research.

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Reactive oxidants regulate membrane repolarization and store-operated uptake of calcium by formyl peptide-activated human neutrophils

Cited by 15 publications

References 25 publications

Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca2+/c-Abl signaling pathway

Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca2+/c-Abl signaling pathway

Redox regulation of calcium ion channels: Chemical and physiological aspects

Vascular and Cellular Calcium in Normal and Hypertensive Pregnancy

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