Hydrogen Peroxide Induces Intracellular Calcium Overload by Activation of a Non-selective Cation Channel in an Insulin-secreting Cell Line

Herson, Paco S.; Lee, Kevin; Pinnock, R.D.; Hughes, J.; Ashford, M. L. J.

doi:10.1074/jbc.274.2.833

Cited by 107 publications

(75 citation statements)

References 47 publications

(45 reference statements)

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“…The typical profile of the intracellular calcium response identified in our study has also been observed in other cell lines exposed to H 2 O 2 , such as HeLa, human erythrocytes and MDCK (a canine epithelial cell line) [53], CRI-G1 (an insulin-secreting cell line) [54] or pancreatic acinar cells [14,55]. However, to our knowledge, this is the first time this effect has been demonstrated in MCF-7 cells.…”

Section: Discussionsupporting

confidence: 85%

Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells

Dejeans

Tajeddine

Beck

et al. 2010

Biochemical Pharmacology

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Please cite this article as: Dejeans N, Tajeddine N, Beck R, Verrax J, Taper H, Gailly P, Calderon PB, Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells, Biochemical Pharmacology (2008), doi:10.1016/j.bcp.2009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 2 ABSTRACTIncrease in cytosolic calcium concentration ([Ca 2+ ] c ), release of endoplasmic reticulum (ER) calcium ([Ca 2+ ] er ) and ER stress have been proposed to be involved in oxidative toxicity.Nevertheless, their relative involvements in the processes leading to cell death are not well defined. In this study, we investigated whether oxidative stress generated during ascorbatedriven menadione redox cycling (Asc/Men) could trigger these three events, and, if so, A c c e p t e d M a n u s c r i p t 3 IntroductionIt has long been known that disruption of intracellular calcium homeostasis is one of the primary processes in the early development of cell injury [1][2][3] [19,[24][25][26][27][28]. In summary, ER homeostasis is a fragile equilibrium, which can be modulated by dysregulation of calcium or oxidative/reductive balance, features previously associated with oxidative stress. However, studies of the links between these factors are scarce.We and others have shown that the association of ascorbate and menadione is an H 2 O 2 -generating system that results in necrosis-like cell death in a wide variety of cancer cell types [29][30][31][32][33][34][35] including MCF-7 cells (a human breast derived cell line), and that loss of calcium homeostasis appeared to be a major factor in the cytotoxicity [36]. The aim of the present study was to investigate the role of disruption of calcium homeostasis and a potential involvement of ER stress in the mechanisms leading to cancer cell death from an oxidative Materials and methods ChemicalsMenadione sodium bisulfite (Men), sodium ascorbate ( Cell Culture and TreatmentsThe MCF-7 cell line was a gift from Dr. F. Brasseur (Ludwig Institute for Cancer Research, LICR-Brussels). The cells were cultured in DMEM (Dulbecco's modified eagle medium, (Gibco BRL, Life Technologies, Merelbeke, BE)) supplemented with 10% fetal calf serum, penicillin (10 000 U/ml), streptomycin (10 mg/ml) and 1.2% glutamine. The cultures were maintained at a density of about 50x10³ cells/cm². The medium was changed at 48-72 h intervals. All cultures were maintained at 37°C in 95% air/5% CO2 with 100% humidity. minutes before the addition of ascorbate and menadione. Cells were incubated with TG or iodoacetate at concentration...

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Section: Discussionsupporting

confidence: 85%

Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells

Dejeans

Tajeddine

Beck

et al. 2010

Biochemical Pharmacology

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“…2,[7][8][9] Transient receptor potential M2 (TRPM2) channels were initially identified and extensively characterized by our group, 7,8,10,11 and demonstrated to contribute to oxidative stress-induced cell death. Indeed, the most well-characterized role for TRPM2 is as an executioner of cell death after oxidative stress, leading to excessive Ca 2 þ influx and consequent cell death (For review, see 1,2,9,12,13 ).…”

Section: Introductionmentioning

confidence: 99%

Androgen and PARP-1 Regulation of TRPM2 Channels after Ischemic Injury

Shimizu

Macey

Quillinan

et al. 2013

J Cereb Blood Flow Metab

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The calcium-permeable transient receptor potential M2 (TRPM2) ion channel was recently demonstrated to have a sexually dimorphic contribution to ischemic brain injury, with inhibition or knockdown of the channel protecting male brain preferentially. We tested the hypothesis that androgen signaling is required for this male-specific cell-death pathway. Additionally, we tested the hypothesis that differential activation of the enzyme poly (ADP-ribose) polymerase-1 (PARP-1) is responsible for male-specific TRPM2 channel activation and neuronal injury. We observed that administration of the TRPM2 inhibitor clotrimazole (CTZ) 2 hours after onset of ischemia reduced infarct volume in male mice and that protection from ischemic damage by CTZ was abolished by removal of testicular androgens (castration; CAST) and rescued by androgen replacement. Male PARP-1 knockout mice had reduced ischemic damage compared with WT mice and inhibition of TRPM2 with CTZ failed to reduce infarct size. Lastly, we observed that ischemia increased PARP activity in the peri-infarct region of male mice to a greater extent than female mice and the difference was abolished in CAST male mice. Data presented in the current study indicate that TRPM2-mediated neuronal death in the male brain requires intact androgen signaling and PARP-1 activity.

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“…The ROS-mediated necrotic volume increase and Na ϩ influx are suggested to be initiated by the binding of the free radicals to ion channels including nonselective Ca 2ϩ channels (10,83,84,105). The increased levels of Na ϩ activates Na ϩ -K ϩ -ATPase and consumes ATP, which further activates nonselective Ca 2ϩ channels, resulting in massive cytosolic Ca 2ϩ accumulation.…”

Section: Ca 2ϩ Accumulationmentioning

confidence: 99%

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

Padanilam

2003

American Journal of Physiology-Renal Physiology

334

268

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In humans and experimental models of renal ischemia, tubular cells in various nephron segments undergo necrotic and/or apoptotic cell death. Various factors, including nucleotide depletion, electrolyte imbalance, reactive oxygen species, endonucleases, disruption of mitochondrial integrity, and activation of various components of the apoptotic machinery, have been implicated in renal cell vulnerability. Several approaches to limit the injury and augment the regeneration process, including nucleotide repletion, administration of growth factors, reactive oxygen species scavengers, and inhibition of inducers and executioners of cell death, proved to be effective in animal models. Nevertheless, an effective approach to limit or prevent ischemic renal injury in humans remains elusive, primarily because of an incomplete understanding of the mechanisms of cellular injury. Elucidation of cell death pathways in animal models in the setting of renal injury and extrapolation of the findings to humans will aid in the design of potential therapeutic strategies. This review evaluates our understanding of the molecular signaling events in apoptotic and necrotic cell death and the contribution of various molecular components of these pathways to renal injury.

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Hydrogen Peroxide Induces Intracellular Calcium Overload by Activation of a Non-selective Cation Channel in an Insulin-secreting Cell Line

Cited by 107 publications

References 47 publications

Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells

Endoplasmic reticulum calcium release potentiates the ER stress and cell death caused by an oxidative stress in MCF-7 cells

Androgen and PARP-1 Regulation of TRPM2 Channels after Ischemic Injury

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

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