Oxidant-induced inhibition of the plasma membrane Ca<sup>2+</sup>-ATPase in pancreatic acinar cells: role of the mitochondria

Baggaley, Erin; Elliott, A.; Bruce, Jason I.E.

doi:10.1152/ajpcell.00083.2008

Cited by 46 publications

(65 citation statements)

References 61 publications

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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: Involvement Of Er Calcium Emptying In Er Stress Triggered Bysupporting

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: Involvement Of Er Calcium Emptying In Er Stress Triggered Bysupporting

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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“…Cell Isolation-Pancreatic acinar cells from Sprague-Dawley rats were isolated by collagenase digestion as previously described (5,6). For all of the fluorescence imaging experiments, the cells were perfused with a HEPES-buffered physiological saline solution (HEPES-PSS; 137 mM Na 5.5 mM glucose, pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

“…We have previously reported that oxidative stress, induced by H 2 O 2 , profoundly altered hormone-evoked [Ca 2ϩ ] i signaling and resulted in an irreversible Ca 2ϩ overload and a marked inhibition of the plasma membrane Ca 2ϩ -ATPase (PMCA) 3 in pancreatic acinar cells (5,6). Although oxidative stress can affect many Ca 2ϩ transport/signaling pathways, the PMCA has an especially key role as the final "gatekeeper" for the control of resting [Ca 2ϩ ] i , especially in cells in which the Na ϩ -Ca 2ϩ exchange is not expressed (7).…”

mentioning

confidence: 99%

Insulin Protects Pancreatic Acinar Cells from Cytosolic Calcium Overload and Inhibition of Plasma Membrane Calcium Pump

Mankad

James

Siriwardena

et al. 2012

Journal of Biological Chemistry

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Background: Impaired metabolism and cytosolic Ca 2ϩ overload in pancreatic acinar cells can trigger pancreatitis. Results: Insulin protected cells from oxidant-induced Ca 2ϩ overload, inhibition of the plasma membrane calcium pump (PMCA), and ATP depletion. Conclusion: Insulin switches metabolism toward glycolysis and fuels the PMCA even when mitochondria are impaired. Significance: This mechanism may provide an important therapeutic strategy for pancreatitis.

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“…Thus, achievement of high mitochondrial Ca 2+ levels under oxidative stress has been pointed out as the major factor determining mitochondria-dependent cell fate (Baumgartner et al, 2009). The implication of mitochondria in the impairment of the normal spatiotemporal pattern of intracellular Ca 2+ signaling and, in particular, the transition to an irreversible intracellular Ca 2+ overload has also been suggested (Baggaley et al, 2008).…”

Section: Mitochondria and Oxidative Stressmentioning

confidence: 99%

Melatonin, mitochondria, and Ca2+ homeostasis in the exocrine pancreas: an overview

González¹,

Santofimia-Castaã'o²,

Salido³

2015

Turk J Biol

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Melatonin, a derivative of the amino acid tryptophan, was initially thought to be mainly produced and secreted by the pineal gland; with time, it was also found in other tissues and organs, and even in plants. Since its discovery, the study of the role of the indole in cellular homeostasis has generated impressive data, which have led researchers to a common idea regarding the positive actions of melatonin in health. The uncontrolled production of free radicals in cellular systems leads to the situation termed oxidative stress, which has been signaled as the basis of disease and aging. In the exocrine pancreas, as in other parts of the body, a daily confrontation takes place against oxidative stress. The major signaling mechanisms controlling the physiology of the gland are affected under this situation. Because a love-hate relationship involving mitochondria and oxidative stress has been considered the basis of disease, any physiological regulator that sets hands on the system as a pacemaker will be determinant for the health's fate. Here we present an overview of the recent findings regarding the protective role of melatonin on the function of the exocrine pancreas, paying attention to the role of Ca2+ signaling and the involvement of mitochondria.

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Oxidant-induced inhibition of the plasma membrane Ca²⁺-ATPase in pancreatic acinar cells: role of the mitochondria

Cited by 46 publications

References 61 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

Insulin Protects Pancreatic Acinar Cells from Cytosolic Calcium Overload and Inhibition of Plasma Membrane Calcium Pump

Melatonin, mitochondria, and Ca2+ homeostasis in the exocrine pancreas: an overview

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Oxidant-induced inhibition of the plasma membrane Ca2+-ATPase in pancreatic acinar cells: role of the mitochondria

Cited by 46 publications

References 61 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

Insulin Protects Pancreatic Acinar Cells from Cytosolic Calcium Overload and Inhibition of Plasma Membrane Calcium Pump

Melatonin, mitochondria, and Ca2+ homeostasis in the exocrine pancreas: an overview

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Oxidant-induced inhibition of the plasma membrane Ca²⁺-ATPase in pancreatic acinar cells: role of the mitochondria