ArticleProceedings of the National Academy of Sciences of the United States of America2005
Carbonic anhydrase isozyme-II-deficient mice lack the duodenal bicarbonate secretory response to prostaglandin E2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Carbonic Anhydrases II and IX in Non-ampullary Duodenal Adenomas and Adenocarcinoma.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Article
- Article
- Genetic ablation of carbonic anhydrase IX disrupts gastric barrier function via claudin-18 downregulation and acid backflux.Acta physiologica (Oxford, England) · 2018Article
- Data Mining FAERS to Analyze Molecular Targets of Drugs Highly Associated with Stevens-Johnson Syndrome.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2015Article
- Carbonic anhydrase 2 deficiency leads to increased pyelonephritis susceptibility.American journal of physiology. Renal physiology · 2014Article
- Gene expression profiling in the submandibular gland, stomach, and duodenum of CAVI-deficient mice.Transgenic research · 2011Article
- Pharmacological correction of a defect in PPAR-gamma signaling ameliorates disease severity in Cftr-deficient mice.Nature medicine · 2010Article
- Duodenal acidity "sensing" but not epithelial HCO3- supply is critically dependent on carbonic anhydrase II expression.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- A systematic quantification of carbonic anhydrase transcripts in the mouse digestive system.BMC molecular biology · 2007Article
- Epithelial carbonic anhydrases facilitate PCO2 and pH regulation in rat duodenal mucosa.The Journal of physiology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duodenal bicarbonate secretion (DBS) is accepted as the primary mucosal defense against acid discharged from the stomach and is impaired in patients with duodenal ulcer disease. The secretory response to luminal acid is the main physiological stimulus for DBS and involves mediation by PGE2 produced by mucosal cells. The aim of this investigation is to elucidate the role of carbonic anhydrases (CAs) II and IX in PGE2-mediated bicarbonate secretion in the murine duodenum. CA II- and IX-deficient mice and different combinations of their heterozygous and WT counterparts were studied. A 10-mm segment of the proximal duodenum with intact blood supply was isolated, and DBS was titrated by pH-stat (TitroLine-easy, Schott, Mainz, Germany). Mean arterial blood pressure (MAP) was continuously recorded, and blood acid/base balance and gastrointestinal morphology were analyzed. The duodenal segment spontaneously secreted HCO3(-) at a steady basal rate of 5.3 +/- 0.6 micromol x cm(-1) x h(-1). Perfusing the duodenal lumen for 20 min with 47 microM PGE2 caused a significant increase in DBS to 13.0 +/- 2.9 micromol x cm(-1) x h(-1), P < 0.0001. The DBS response to PGE2 was completely absent in Car2-/- mice, whereas basal DBS was normal. The CA IX-deficient mice with normal Car2 alleles showed a slight increase in DBS. Histological abnormalities were observed in the gastroduodenal epithelium in both CA II- and IX-deficient mice. Our data demonstrate a gastrointestinal phenotypic abnormality associated with CA II deficiency. The results show that the stimulatory effect of the duodenal secretagogue PGE2 completely depends on CA II.
Indexed as
Identifiers
What OpenQuestion holds
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.