Vanadate Induces Calcium Signaling, Ca2+ Release-Activated Ca2+ Channel Activation, and Gene Expression in T Lymphocytes and RBL-2H3 Mast Cells Via Thiol Oxidation

Ehring, George R.; Kerschbaum, Hubert; Fanger, Christopher M.; Eder, Claudia; Rauer, Heiko; Cahalan, Michael D.

doi:10.4049/jimmunol.164.2.679

Cited by 32 publications

(12 citation statements)

References 72 publications

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“…In this regard, both InsP 3 receptors (44) and ryanodine receptors (37) have been identified in colon crypts, the former having also been shown to support Ca 2ϩ -dependent anion secretion (37). In other tissues, functional modification of either receptor has been demonstrated after exposure to thiol oxidants (14,45), the latter in response to chloramines (14). These considerations suggest that NH 2 Cl may find a broad spectrum of targets in the apparatus that regulates store emptying.…”

Section: Discussionmentioning

confidence: 96%

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Cima¹,

Dubach²,

Wieland³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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During acute exacerbations of inflammatory bowel diseases, oxidants are generated through the interactions of bacteria in the lumen, activated granulocytes, and cells of the colon mucosa. In this study we explored the ability of one such class of oxidants, represented by monochloramine (NH(2)Cl), to serve as agonists of Ca(2+) and Zn(2+) accumulation within the colonocyte. Individual colon crypts prepared from Sprague-Dawley rats were mounted in perfusion chambers after loading with fluorescent reporters fura 2-AM and fluozin 3-AM. These reporters were characterized, in situ, for responsiveness to Ca(2+) and Zn(2+) in the cytoplasm. Responses to different concentrations of NH(2)Cl (50, 100, and 200 microM) were monitored. Subsequent studies were designed to identify the sources and mechanisms of NH(2)Cl-induced increases in Ca(2+) and Zn(2+) in the cytoplasm. Exposure to NH(2)Cl led to dose-dependent increases in intracellular Ca(2+) concentration ([Ca(2+)](i)) in the range of 200-400 nM above baseline levels. Further studies indicated that NH(2)Cl-induced accumulation of Ca(2+) in the cytoplasm is the result of release from intracellular stores and basolateral entry of extracellular Ca(2+) through store-operated channels. In addition, exposure to NH(2)Cl resulted in dose-dependent and sustained increases in intracellular Zn(2+) concentration ([Zn(2+)](i)) in the nanomolar range. These alterations were neutralized by dithiothreitol, which shields intracellular thiol groups from oxidation. We conclude that Ca(2+)- and Zn(2+)-handling proteins are susceptible to oxidation by chloramines, leading to sustained, but not necessarily toxic, increases in [Ca(2+)](i) and [Zn(2+)](i). Under certain conditions, NH(2)Cl may act not as a toxin but as an agent that activates intracellular signaling pathways.

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Section: Discussionmentioning

confidence: 96%

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Cima¹,

Dubach²,

Wieland³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Indeed, several studies showed that maintenance of SOCE can be modulated by redox induced changes in phosphorylation [14,178,179]. 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].…”

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

confidence: 99%

“…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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“…The number of studies establishing that exposure to oxidants increases SOCE by favoring ER Ca 2 + depletion (50,81,130,145,153,192) and more recently (70) are nearly matched by those supporting a role for ROS in diminishing SOCE (59, 173, 191, 215), while others still report time-, dose-, and reactive species-dependent effects (52,159,160). As our understanding of SOCE has grown since the discovery of STIM and Orai proteins, it is likely that one of the major reasons underlying these discrepancies are cell-type differences, since the SOCE machinery changes depending on cell type.…”

Section: Redox Control Of the Core Soce Machinerymentioning

confidence: 99%

Redox Regulation of Store-Operated Ca²⁺Entry

Nunes

Demaurex

2014

Antioxidants & Redox Signaling

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Significance: Store-operated Ca 2+ entry (SOCE) is a ubiquitous Ca 2+ signaling mechanism triggered by Ca 2+ depletion of the endoplasmic reticulum (ER) and by a variety of cellular stresses. Reactive oxygen species (ROS) are often concomitantly produced in response to these stresses, however, the relationship between redox signaling and SOCE is not completely understood. Various cardiovascular, neurological, and immune diseases are associated with alterations in both Ca 2+ signaling and ROS production, and thus understanding this relationship has therapeutic implications. Recent Advances: Several reactive cysteine modifications in stromal interaction molecule (STIM) and Orai proteins comprising the core SOCE machinery were recently shown to modulate SOCE in a redox-dependent manner. Moreover, STIM1 and Orai1 expression levels may reciprocally regulate and be affected by responses to oxidative stress. ER proteins involved in oxidative protein folding have gained increased recognition as important sources of ROS, and the recent discovery of their accumulation in contact sites between the ER and mitochondria provides a further link between ROS production and intracellular Ca 2+ handling. Critical Issues and Future Directions: Future research should aim to establish the complete set of SOCE controlling molecules, to determine their redox-sensitive residues, and to understand how intracellular Ca 2+ stores dynamically respond to different types of stress. Mapping the precise nature and functional consequence of key redox-sensitive components of the pre-and post-translational control of SOCE machinery and of proteins regulating ER calcium content will be pivotal in advancing our understanding of the complex crosstalk between redox and Ca 2+ signaling. Antioxid. Redox Signal. 21, 915-932.

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Vanadate Induces Calcium Signaling, Ca2+ Release-Activated Ca2+ Channel Activation, and Gene Expression in T Lymphocytes and RBL-2H3 Mast Cells Via Thiol Oxidation

Cited by 32 publications

References 72 publications

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Redox regulation of calcium ion channels: Chemical and physiological aspects

Redox Regulation of Store-Operated Ca²⁺Entry

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Vanadate Induces Calcium Signaling, Ca2+ Release-Activated Ca2+ Channel Activation, and Gene Expression in T Lymphocytes and RBL-2H3 Mast Cells Via Thiol Oxidation

Cited by 32 publications

References 72 publications

Intracellular Ca2+and Zn2+signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Intracellular Ca2+and Zn2+signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Redox regulation of calcium ion channels: Chemical and physiological aspects

Redox Regulation of Store-Operated Ca2+Entry

Contact Info

Product

Resources

About

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Intracellular Ca²⁺and Zn²⁺signals during monochloramine-induced oxidative stress in isolated rat colon crypts

Redox Regulation of Store-Operated Ca²⁺Entry