ArticlePflugers Archiv : European journal of physiology2009
Ducts isolated from the pancreas of CFTR-null mice secrete fluid.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Ion Channel Signature in Healthy Pancreas and Pancreatic Ductal Adenocarcinoma.Frontiers in pharmacology · 2020Review
- The Importance of Aquaporin 1 in Pancreatitis and Its Relation to the CFTR ClFrontiers in physiology · 2018Article
- Novel Insight Into the Role of CFTR in Lacrimal Gland Duct Function in Mice.Investigative ophthalmology & visual science · 2018Article
- Article
- Animal models of gastrointestinal and liver diseases. Animal models of cystic fibrosis: gastrointestinal, pancreatic, and hepatobiliary disease and pathophysiology.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- Ferret and pig models of cystic fibrosis: prospects and promise for gene therapy.Human gene therapy. Clinical development · 2015Review
- Acid-base transport in pancreas-new challenges.Frontiers in physiology · 2013Review
- The physiological roles of secretin and its receptor.Annals of translational medicine · 2013Review
- The cystic fibrosis of exocrine pancreas.Cold Spring Harbor perspectives in medicine · 2013Review
- Deletion of Slc26a6 alters the stoichiometry of apical Cl-/HCO-3 exchange in mouse pancreatic duct.American journal of physiology. Cell physiology · 2012Article
- New animal models of cystic fibrosis: what are they teaching us?Current opinion in pulmonary medicine · 2011Review
- Chloride transport in microperfused interlobular ducts isolated from guinea-pig pancreas.The Journal of physiology · 2002Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The pancreatic pathology in cystic fibrosis (CF) is normally attributed to the failure of ductal fluid secretion resulting from the lack of functional CF transmembrane conductance regulator (CFTR). However, murine models of CF show little or no pancreatic pathology. To resolve this dichotomy we analysed the transport mechanisms involved in fluid and electrolyte secretion by pancreatic ducts isolated from CFTR-null mice. Experiments were performed on cultured interlobular duct segments isolated from the pancreas of the Cftr(tm1Cam) strain of CFTR-null mouse. Fluid secretion to the closed luminal space was measured by video microscopy. The secretory response of ducts isolated from CF mice to cAMP-elevating agonists forskolin and secretin was significantly reduced compared with wild type but not abolished. The Cl(-)- and HCO(3) (-) -dependent components of the ductal secretion were affected equally by the absence of CFTR. The secretory response to carbachol stimulation was unaltered in CF ducts. Loading the ductal cells with the Ca2+ chelator BAPTA completely abolished carbachol-evoked secretion, but did not affect forskolin-evoked secretion in CF or wild-type ducts. We conclude that pancreatic duct cells from CF mice can secrete a significant amount of water and electrolytes by a cAMP-stimulated mechanism that is independent of CFTR and cannot be ascribed to the activation of calcium-activated chloride channels.
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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.