ArticleThe Journal of biological chemistry2013
Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies.World journal of gastroenterology · 2025Review
- Review
- Pancreatic involvement inMolecular genetics and metabolism reports · 2025Article
- Gut microbiota analysis and LC-MS-based metabolomics to investigate AMPK/NF-κB regulated by Clostridium butyricum in the treatment of acute pancreatitis.Journal of translational medicine · 2024Article
- Long-chain fatty acids - The turning point between 'mild' and 'severe' acute pancreatitis.Heliyon · 2024Review
- Discoveries of GPR39 as an evolutionarily conserved receptor for bile acids and of its involvement in biliary acute pancreatitis.Science advances · 2024Article
- The Role of Bile Acids in Pancreatic Cancer.Current cancer drug targets · 2024Review
- Cofilin activation in pancreatic acinar cells plays a pivotal convergent role for mediating CCK-stimulated enzyme secretion and growth.Frontiers in physiology · 2023Article
- Investigation of the potential role of TGR5 in pancreatic cancer by a comprehensive molecular experiments and the liquid chromatography mass spectrometry (LC-MS) based metabolomics.Discover oncology · 2022Article
- New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice.Journal of veterinary internal medicine · 2022Review
- Intracellular CaInternational journal of molecular sciences · 2020Review
- TMEM16A CaJournal of advanced research · 2020Article
- PKC Mediates LPS-Induced IL-1β Expression and Participates in the Pro-inflammatory Effect of ANeurochemical research · 2019Article
- The Orai CaThe Journal of physiology · 2019Article
- Region-specific proteolysis differentially modulates type 2 and type 3 inositol 1,4,5-trisphosphate receptor activity in models of acute pancreatitis.The Journal of biological chemistry · 2018Article
- High expression of TGR5 predicts a poor prognosis in patients with pancreatic cancer.International journal of clinical and experimental pathology · 2018Article
- Acinar injury and early cytokine response in human acute biliary pancreatitis.Scientific reports · 2017Article
- Bone marrow-derived mesenchymal stem cells (BMSCs) repair acute necrotized pancreatitis by secreting microRNA-9 to target the NF-κB1/p50 gene in rats.Scientific reports · 2017Article
- Role of bile acids in carcinogenesis of pancreatic cancer: An old topic with new perspective.World journal of gastroenterology · 2016Review
- TRAM1 protects AR42J cells from caerulein-induced acute pancreatitis through ER stress-apoptosis pathway.In vitro cellular & developmental biology. Animal · 2016Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Biliary pancreatitis is the most common etiology of acute pancreatitis, accounting for 30-60% of cases. A dominant theory for the development of biliary pancreatitis is the reflux of bile into the pancreatic duct and subsequent exposure to pancreatic acinar cells. Bile acids are known to induce aberrant Ca(2+) signals in acinar cells as well as nuclear translocation of NF-κB. In this study, we examined the role of the downstream Ca(2+) target calcineurin on NF-κB translocation. Freshly isolated mouse acinar cells were infected for 24 h with an adenovirus expressing an NF-κB luciferase reporter. The bile acid taurolithocholic acid-3-sulfate caused NF-κB activation at concentrations (500 μm) that were associated with cell injury. We show that the NF-κB inhibitor Bay 11-7082 (1 μm) blocked translocation and injury. Pretreatment with the Ca(2+) chelator 1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from calcineurin Aβ-deficient mice each led to reduced NF-κB activation with taurolithocholic acid-3-sulfate. Importantly, these manipulations did not affect LPS-induced NF-κB activation. A critical upstream regulator of NF-κB activation is protein kinase C, which translocates to the membranes of various organelles in the active state. We demonstrate that pharmacologic and genetic inhibition of calcineurin blocks translocation of the PKC-δ isoform. In summary, bile-induced NF-κB activation and acinar cell injury are mediated by calcineurin, and a mechanism for this important early inflammatory response appears to be upstream at the level of PKC translocation.
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Registered trials
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.