ROS and Ca 2+ —Partners in sickness and in health

Ambudkar, Indu S.; Muallem, Shmuel

doi:10.1016/j.ceca.2016.06.003

Cited by 8 publications

(6 citation statements)

References 48 publications

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“…To substantiate the reversal claim, the MSCs coculture drastically reduced basal elevated [Ca 2+ ] i and, subsequently, ROS. Inflammatory-cell rescue to normal or near-normal levels has been reported previously by many studies, including ours [10,60,61,62] with more emphasis on mitochondrial involvement. It should be noted that ROS and calcium interactions are bidirectional, as calcium is essential for ROS promotion, while the latter are a potent regulator of calcium signals [63].…”

Section: Discussionsupporting

confidence: 82%

Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Alhazzani

Rajagopalan

Albarqi

et al. 2018

Cells

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Cell-therapy modalities using mesenchymal stem (MSCs) in experimental strokes are being investigated due to the role of MSCs in neuroprotection and regeneration. It is necessary to know the sequence of events that occur during stress and how MSCs complement the rescue of neuronal cell death mediated by [Ca2+]i and reactive oxygen species (ROS). In the current study, SH-SY5Y-differentiated neuronal cells were subjected to in vitro cerebral ischemia-like stress and were experimentally rescued from cell death using an MSCs/neuronal cell coculture model. Neuronal cell death was characterized by the induction of proinflammatory tumor necrosis factor (TNF)-α, interleukin (IL)-1β and -12, up to 35-fold with corresponding downregulation of anti-inflammatory cytokine transforming growth factor (TGF)-β, IL-6 and -10 by approximately 1 to 7 fold. Increased intracellular calcium [Ca2+]i and ROS clearly reaffirmed oxidative stress-mediated apoptosis, while upregulation of nuclear factor NF-κB and cyclo-oxygenase (COX)-2 expressions, along with ~41% accumulation of early and late phase apoptotic cells, confirmed ischemic stress-mediated cell death. Stressed neuronal cells were rescued from death when cocultured with MSCs via increased expression of anti-inflammatory cytokines (TGF-β, 17%; IL-6, 4%; and IL-10, 13%), significantly downregulated NF-κB and proinflammatory COX-2 expression. Further accumulation of early and late apoptotic cells was diminished to 23%, while corresponding cell death decreased from 40% to 17%. Low superoxide dismutase 1 (SOD1) expression at the mRNA level was rescued by MSCs coculture, while no significant changes were observed with catalase (CAT) and glutathione peroxidase (GPx). Interestingly, increased serotonin release into the culture supernatant was proportionate to the elevated [Ca2+]i and corresponding ROS, which were later rescued by the MSCs coculture to near normalcy. Taken together, all of these results primarily support MSCs-mediated modulation of stressed neuronal cell survival in vitro.

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Section: Discussionsupporting

confidence: 82%

Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Alhazzani

Rajagopalan

Albarqi

et al. 2018

Cells

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“…Together with reactive nitrogen species (RNS), calcium ions and others, these are universal signaling species in cells. [2][3][4][5][6][7][8][9][10][11][12] In principle, H 2 O 2 is formed by a sequential 2e¯transfer to O 2 , whereby the intermediate radical • O 2¯i s produced. • O 2¯i s subsequently protonated resulting in the nonradical H 2 O 2 .…”

Section: Redox Chemistry Of Hydrogen Peroxidementioning

confidence: 99%

“…RM ox + 2e¯→ RM red [5] metalloprotein ox + RM red → metalloprotein red + RM ox [6] metalloprotein red + H 2 O 2 + 2H + → 2H 2 O + metalloprotein ox [7] Overall reaction:…”

Section: G87mentioning

confidence: 99%

“…Another report described an amperometric sensor for H 2 O 2 based on a combined modification with porous nickel hydroxide and cytochrome c. 256 Redox mediators.-Functioning of protein-based electrochemical sensors can be improved further by addition of soluble or surfaceimmobilized redox mediators to the aqueous electrolyte solution, such as hexacyanoferrates, ferrocene derivatives, methylene blue or quinones. 257 Figure 4 summarizes the structural composition of the modified electrode surface (Figure 4A), and the sequence of redox Reactions (5, 6, 7; see below) at a (metallo) protein-modified electrode for H 2 O 2 determination in the presence of a surface immobilized redox mediator (RM), and in a deoxygenated solution, assuming a reductive electrode mechanism (Figure 4C; metalloprotein ox = OP and metalloprotein red = RP): RM ox + 2e¯→ RM red [5] metalloprotein ox + RM red → metalloprotein red + RM ox [6] metalloprotein red + H 2 O 2 + 2H + → 2H 2 O + metalloprotein ox [7] Overall reaction:…”

Section: Electrochemical Determination and Quantification Of H 2 Omentioning

confidence: 99%

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Review—Quantification of Hydrogen Peroxide by Electrochemical Methods and Electron Spin Resonance Spectroscopy

Gulaboski

Mirčeski

Kappl

et al. 2019

J. Electrochem. Soc.

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Reactive oxygen species (ROS) exhibit different spatial and temporal distributions as well as concentrations in-and outside the cell, thereby functioning as signaling or pathogen-destroying molecules. Especially the ROS H 2 O 2 is important for the patho/physiological status of an organism. Electrochemistry (EM) and electron spin resonance (ESR)-based techniques allow quantification of H 2 O 2 in artificial and living systems, coping a concentration range from low nM up to mM. Working electrodes for EM are optimized by diverse modifications and, additionally, redox mediators are used. Ultramicroelectrodes allow scanning of single cells to spatially resolve and quantify extracellular H 2 O 2 in real-time. With ESR spectroscopy, • O 2¯, but not H 2 O 2 , can be directly determined by spin probes in-and outside of cells in suspensions. Monitoring H 2 O 2 requires formation of intermediate radicals, detectable with spin probes. Low μM [H 2 O 2 ] can thus be assessed specifically. Using suitable spin traps, in-vivo ESR and immuno-spin trapping can visualize different radicals at their respective production sites in small animals, organs and tissues. Here, the redox reaction cascades may interfere with cell metabolism. Optimization of all methods established for H 2 O 2 determination would be favorable to finally combine them for mutual validation. Thus, a deeper insight into cellular ROS metabolism can be obtained.

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“…Excessive Ca 2+ influx results in accumulation of Ca 2+ in the mitochondria of salivary gland cells [123], enterocytes [124], hepatocytes [125] and pancreatic acinar [46] and stellate cells [126]. The Ca 2+ overload causes excessive mitochondrial ROS generation, cell damage and cell death [127][128][129]. Chronic excessive ROS has several deleterious effects.…”

Section: Ca 2+ Influx In Secretory Glands Pathologymentioning

confidence: 99%

CRAC channels in secretory epithelial cell function and disease

Kabrah

Ahuja

et al. 2019

Cell Calcium

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The receptor-evoked Ca 2+ signal in secretory epithelia mediate many cellular functions essential for cell survival and their most fundamental functions of secretory granules exocytosis and fluid and electrolyte secretion. Ca 2+ influx is a key component of the receptor-evoked Ca 2+ signal in secretory cell and is mediated by both TRPC and the STIM1-activated Orai1 channels that mediates the Ca 2+ release-activated current (CRAC) I crac . The core components of the receptorevoked Ca 2+ signal are assembled at the ER/PM junctions where exchange of materials between the plasma membrane and internal organelles take place, including transfer of lipids and Ca 2+ . The Ca 2+ signal generated at the confined space of the ER/PM junctions is necessary for activation of the Ca 2+ -regulated proteins and ion channels that mediate exocytosis with high fidelity and tight control. In this review we discuss the general properties of Ca 2+ signaling, PI(4,5)P 2 and other lipids at the ER/PM junctions with regard to secretory cells function and disease caused by uncontrolled Ca 2+ influx.

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ROS and Ca 2+ —Partners in sickness and in health

Cited by 8 publications

References 48 publications

Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Mesenchymal Stem Cells (MSCs) Coculture Protects [Ca2+]i Orchestrated Oxidant Mediated Damage in Differentiated Neurons In Vitro

Review—Quantification of Hydrogen Peroxide by Electrochemical Methods and Electron Spin Resonance Spectroscopy

CRAC channels in secretory epithelial cell function and disease

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