ArticleAmerican journal of physiology. Cell physiology2008
Oxidant-induced inhibition of the plasma membrane Ca2+-ATPase in pancreatic acinar cells: role of the mitochondria.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026Review
- Kinetics of the thapsigargin-induced CaFrontiers in physiology · 2023Article
- Peripheral biomarkers of oxidative stress in dogs with acute pancreatitis.Journal of veterinary internal medicine · 2022Article
- Research Progress of Antioxidant Nanomaterials for Acute Pancreatitis.Molecules (Basel, Switzerland) · 2022Review
- The modulation of ion channels in cancer chemo-resistance.Frontiers in oncology · 2022Review
- Insulin protects acinar cells during pancreatitis by preserving glycolytic ATP supply to calcium pumps.Nature communications · 2021Article
- Resveratrol derivatives increase cytosolic calcium by inhibiting plasma membrane ATPase and inducing calcium release from the endoplasmic reticulum in prostate cancer cells.Biochemistry and biophysics reports · 2019Article
- CRAC channels in secretory epithelial cell function and disease.Cell calcium · 2019Review
- Galactose protects against cell damage in mouse models of acute pancreatitis.The Journal of clinical investigation · 2018Article
- Oxidative stress alters mitochondrial bioenergetics and modifies pancreatic cell death independently of cyclophilin D, resulting in an apoptosis-to-necrosis shift.The Journal of biological chemistry · 2018Article
- Hydrogen peroxide inhibits CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- Glycolysis is essential for chemoresistance induced by transient receptor potential channel C5 in colorectal cancer.BMC cancer · 2018Article
- Metabolic regulation of the PMCA: Role in cell death and survival.Cell calcium · 2018Review
- Inhibition of Calpains Protects Mn-Induced Neurotransmitter release disorders in Synaptosomes from Mice: Involvement of SNARE Complex and Synaptic Vesicle Fusion.Scientific reports · 2017Article
- Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms.Frontiers in pharmacology · 2017Review
- Calcium and adenosine triphosphate control of cellular pathology: asparaginase-induced pancreatitis elicited via protease-activated receptor 2.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation.Open biology · 2016Article
- The Plasma Membrane Calcium Pump in Pancreatic Cancer Cells Exhibiting the Warburg Effect Relies on Glycolytic ATP.The Journal of biological chemistry · 2015Article
- Redox signaling in acute pancreatitis.Redox biology · 2015Review
- Novel lipophilic probe for detecting near-membrane reactive oxygen species responses and its application for studies of pancreatic acinar cells: effects of pyocyanin and L-ornithine.Antioxidants & redox signaling · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Impairment of the normal spatiotemporal pattern of intracellular Ca(2+) ([Ca(2+)](i)) signaling, and in particular, the transition to an irreversible "Ca(2+) overload" response, has been implicated in various pathophysiological states. In some diseases, including pancreatitis, oxidative stress has been suggested to mediate this Ca(2+) overload and the associated cell injury. We have previously demonstrated that oxidative stress with hydrogen peroxide (H(2)O(2)) evokes a Ca(2+) overload response and inhibition of plasma membrane Ca(2+)-ATPase (PMCA) in rat pancreatic acinar cells (Bruce JI and Elliott AC. Am J Physiol Cell Physiol 293: C938-C950, 2007). The aim of the present study was to further examine this oxidant-impaired inhibition of the PMCA, focusing on the role of the mitochondria. Using a [Ca(2+)](i) clearance assay in which mitochondrial Ca(2+) uptake was blocked with Ru-360, H(2)O(2) (50 microM-1 mM) markedly inhibited the PMCA activity. This H(2)O(2)-induced inhibition of the PMCA correlated with mitochondrial depolarization (assessed using tetramethylrhodamine methylester fluorescence) but could occur without significant ATP depletion (assessed using Magnesium Green fluorescence). The H(2)O(2)-induced PMCA inhibition was sensitive to the mitochondrial permeability transition pore (mPTP) inhibitors, cyclosporin-A and bongkrekic acid. These data suggest that oxidant-induced opening of the mPTP and mitochondrial depolarization may lead to an inhibition of the PMCA that is independent of mitochondrial Ca(2+) handling and ATP depletion, and we speculate that this may involve the release of a mitochondrial factor. Such a phenomenon may be responsible for the Ca(2+) overload response, and for the transition between apoptotic and necrotic cell death thought to be important in many disease states.
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