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

Mankad, Parini; James, Andy; Siriwardena, Ajith K.; Elliott, A.; Bruce, Jason I.E.

doi:10.1074/jbc.m111.326272

Cited by 44 publications

(55 citation statements)

References 56 publications

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“…Any inhibition of [Ca 2+ ] i clearance observed using this experimental design can, therefore, be interpreted as an effect on PMCA activity, consistent with our previous studies (12, 18). …”

Section: Resultssupporting

confidence: 90%

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Glycolytic ATP Fuels the Plasma Membrane Calcium Pump Critical for Pancreatic Cancer Cell Survival

James

Chan

Erice

et al. 2013

Journal of Biological Chemistry

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Background: Pancreatic cancer cells exhibit up-regulated glycolysis.Results: Inhibition of glycolysis, but not mitochondrial metabolism, induced ATP depletion, plasma membrane calcium pump (PMCA) inhibition, Ca2+ overload, and cell death.Conclusion: Glycolytic ATP fuels the PMCA in pancreatic cancer.Significance: Glycolytic regulation of the PMCA may represent a novel chemotherapeutic target for pancreatic cancer.

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Section: Resultssupporting

confidence: 90%

“…PANC1 cells were treated for 0.5–6 h with either BrPy, an inhibitor of the glycolytic enzyme hexokinase (20), or CCCP, a protonophore that collapses the mitochondrial membrane potential (18). …”

Section: Resultsmentioning

confidence: 99%

Glycolytic ATP Fuels the Plasma Membrane Calcium Pump Critical for Pancreatic Cancer Cell Survival

James

Chan

Erice

et al. 2013

Journal of Biological Chemistry

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“…As previously discussed and validated in our previous studies (22, 30), [Ca 2+ ] i clearance under these conditions is almost exclusively due to PMCA activity. Moreover, the paired experimental design controls for both cell-to-cell, and time-dependent, differences in PMCA activity (see Fig.…”

Section: Resultssupporting

confidence: 85%

Insulin Protects Pancreatic Acinar Cells from Palmitoleic Acid-induced Cellular Injury

Samad

James

Wong

et al. 2014

Journal of Biological Chemistry

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Background: Palmitoleic acid is a major pancreatitis-inducing agent.Results: Insulin protected cells from palmitoleic acid (POA)-induced ATP depletion, inhibition of the plasma membrane calcium pump (PMCA), cytotoxic Ca2+ overload and necrosis.Conclusion: Insulin protects against acinar cell injury induced by pancreatitis-inducing agents.Significance: This provides an important therapeutic strategy for treating pancreatitis with insulin therapy.

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“…First, increasing extracellular magnesium reduces pancreatitis responses in rodent acinar cells including pathologic calcium signaling and lessens the severity of in vivo pancreatitis in rodent models113, 114; it now is being examined for its potential role in reducing PEP 112 . Insulin recently was shown to decrease calcium levels caused by induction of pancreatitis responses in acinar cells and reduce other cellular pancreatitis injuries 115, 116. These actions appear to be linked to a plasma-membrane calcium pump.…”

Section: Has Anything Been Identified In Animal Models That Clearly Imentioning

confidence: 99%

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

Gorelick

Lerch

2017

Cellular and Molecular Gastroenterology and Hepatology

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Acute pancreatitis is currently the most common cause of hospital admission among all nonmalignant gastrointestinal diseases. To understand the pathophysiology of the disease and as a potential step toward developing targeted therapies, attempts to induce the disease experimentally began more than 100 years ago. Recent decades have seen progress in developing new experimental pancreatitis models as well as elucidating many underlying cell biological and pathophysiological disease mechanisms. Some models have been developed to reflect specific causes of acute pancreatitis in human beings. However, the paucity of data relating to the molecular mechanisms of human disease, the likelihood that multiple genetic and environmental factors affect the risk of disease development and its severity, and the limited information regarding the natural history of disease in human beings make it difficult to evaluate the value of disease models. Here, we provide an overview of key models and discuss our views on their strengths for characterizing cell biological disease mechanisms or for identifying potential therapeutic targets. We also acknowledge their limitations.

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

Cited by 44 publications

References 56 publications

Glycolytic ATP Fuels the Plasma Membrane Calcium Pump Critical for Pancreatic Cancer Cell Survival

Glycolytic ATP Fuels the Plasma Membrane Calcium Pump Critical for Pancreatic Cancer Cell Survival

Insulin Protects Pancreatic Acinar Cells from Palmitoleic Acid-induced Cellular Injury

Do Animal Models of Acute Pancreatitis Reproduce Human Disease?

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