ArticleProceedings of the National Academy of Sciences of the United States of America2011
Calmodulin protects against alcohol-induced pancreatic trypsinogen activation elicited via Ca2+ release through IP3 receptors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 45 citations in OpenAlex.
- The role of CaCell calcium · 2023Review
- Activation of pancreatic stellate cells attenuates intracellular CaCell death & disease · 2022Article
- Astrocytic IPFrontiers in cellular neuroscience · 2021Review
- TRPV4 channel opening mediates pressure-induced pancreatitis initiated by Piezo1 activation.The Journal of clinical investigation · 2020Article
- BH3 mimetic-elicited CaCell death & disease · 2017Article
- Article
- Alcoholic pancreatitis: New insights into the pathogenesis and treatment.World journal of gastrointestinal pathophysiology · 2016Review
- Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis.World journal of gastroenterology · 2014Review
- The ryanodine receptor is expressed in human pancreatic acinar cells and contributes to acinar cell injury.American journal of physiology. Gastrointestinal and liver physiology · 2014Article
- Article
- The role of Ca2+ in the pathophysiology of pancreatitis.The Journal of physiology · 2014Review
- Cluster of differentiation 38 (CD38) mediates bile acid-induced acinar cell injury and pancreatitis through cyclic ADP-ribose and intracellular calcium release.The Journal of biological chemistry · 2013Article
- Ca2+ release-activated Ca2+ channel blockade as a potential tool in antipancreatitis therapy.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin.The Journal of biological chemistry · 2013Article
- Effects of oxidative alcohol metabolism on the mitochondrial permeability transition pore and necrosis in a mouse model of alcoholic pancreatitis.Gastroenterology · 2013Article
- Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.The Journal of biological chemistry · 2013Article
- Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium.PloS one · 2013Article
- Mitochondrial function and malfunction in the pathophysiology of pancreatitis.Pflugers Archiv : European journal of physiology · 2012Review
- Ryanodine receptors contribute to bile acid-induced pathological calcium signaling and pancreatitis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Physiology and pathophysiology of bicarbonate secretion by pancreatic duct epithelium.Nagoya journal of medical science · 2012Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Alcohol abuse is a major global health problem, but there is still much uncertainty about the mechanisms of action. So far, the effects of ethanol on ion channels in the plasma membrane have received the most attention. We have now investigated actions on intracellular calcium channels in pancreatic acinar cells. Our aim was to discover the mechanism by which alcohol influences calcium homeostasis and thereby understand how alcohol can trigger premature intracellular trypsinogen activation, which is the initiating step for alcohol-induced pancreatitis. We used intact or two-photon permeabilized acinar cells isolated from wild-type mice or mice in which inositol trisphosphate receptors of type 2 or types 2 and 3 were knocked out. In permeabilized pancreatic acinar cells even a relatively low ethanol concentration elicited calcium release from intracellular stores and intracellular trypsinogen activation. The calcium sensor calmodulin (at a normal intracellular concentration) markedly reduced ethanol-induced calcium release and trypsinogen activation in permeabilized cells, effects prevented by the calmodulin inhibitor peptide. A calmodulin activator virtually abolished the modest ethanol effects in intact cells. Both ethanol-elicited calcium liberation and trypsinogen activation were significantly reduced in cells from type 2 inositol trisphosphate receptor knockout mice. More profound reductions were seen in cells from double inositol trisphosphate receptor (types 2 and 3) knockout mice. The inositol trisphosphate receptors, required for normal pancreatic stimulus-secretion coupling, are also responsible for the toxic ethanol action. Calmodulin protects by reducing calcium release sensitivity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.