Evidence map›Paper›PMID 16816370›Full record

ArticleThe American journal of pathology2006

Inefficient chronic activation of parietal cells in Ae2a,b(-/-) mice.

Sergio Recalde, Francisco Muruzábal, Norbert Looije, Cindy Kunne, María A Burrell, Elena Sáez, Eduardo Martínez-Ansó, January T Salas, Pablo Mardones, Jesús Prieto and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. The role of soluble adenylyl cyclase in sensing and regulating intracellular pH.Pflugers Archiv : European journal of physiology · 2024
    Review
  3. Review
  4. Review
  5. Mouse models of SLC4-linked disorders of HCOAmerican journal of physiology. Cell physiology · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Fibrosis in autoimmune and cholestatic liver disease.Best practice & research. Clinical gastroenterology · 2011
    Review
  11. Article
  12. Article
  13. Localization and function of the anion exchanger Ae2 in developing teeth and orofacial bone in rodents.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2009
    Article
  14. Review
  15. HCO3-/Cl- anion exchanger SLC4A2 is required for proper osteoclast differentiation and function.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  16. The anion exchanger Ae2 is required for enamel maturation in mouse teeth.Matrix biology : journal of the International Society for Matrix Biology · 2008
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Sergio RecaldeLaboratory of Experimental Hepatology, Academic Medical Center Liver Center, Amsterdam, The Netherlands.
Francisco Muruzábal
Norbert Looije
Cindy Kunne
María A Burrell
Elena Sáez
Eduardo Martínez-Ansó
January T Salas
Pablo Mardones
Jesús Prieto
Juan F Medina
Ronald P J Oude Elferink
Universidad de Navarra · ESAcademic Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In parietal cells, basolateral Ae2 Cl(-)/HCO(3)(-) exchanger (Slc4a2) appears to compensate for luminal H(+) pumping while providing Cl(-) for apical secretion. In mouse and rat, mRNA variants Ae2a, Ae2b1, Ae2b2, and Ae2c2 are all found in most tissues (although the latter at very low levels), whereas Ae2c1 is restricted to the stomach. We studied the acid secretory function of gastric mucosa in mice with targeted disruption of Ae2a, Ae2b1, and Ae2b2 (but not Ae2c) isoforms. In the oxyntic mucosa of Ae2(a,b)(-/-) mice, total Ae2 protein was nearly undetectable, indicating low gastric expression of the Ae2c isoforms. In Ae2(a,b)(-/-) mice basal acid secretion was normal, whereas carbachol/histamine-stimulated acid secretion was impaired by 70%. These animals showed increased serum gastrin levels and hyperplasia of G cells. Immunohistochemistry and electron microscopy revealed baseline activation of parietal cells with fusion of intracellular H(+)/K(+)-ATPase-containing vesicles with the apical membrane and degenerative changes (but not substantial apoptosis) in a subpopulation of these cells. Increased expression of proliferating cell nuclear antigen in the oxyntic glands suggested enhanced Ae2(a,b)(-/-) parietal cell turnover. These data reveal a critical role of Ae2a-Ae2b1-Ae2b2 isoforms in stimulated gastric acid secretion whereas residual Ae2c isoforms could account to a limited extent for basal acid secretion.

Indexed as

AnimalsAnion Transport ProteinsAntiportersApoptosisBlotting, WesternChloride-Bicarbonate AntiportersGastric AcidGastric MucosaGastrinsGene ExpressionImmunohistochemistryIn Situ Nick-End LabelingMiceMicroscopy, Electron, TransmissionParietal Cells, GastricProtein IsoformsAnion Transport ProteinsAntiportersChloride-Bicarbonate AntiportersGastrinsProtein IsoformsRNA, MessengerSlc4a2 protein, mouseSlc4a2 protein, ratSLC4A Proteins

Identifiers

PMID16816370
PMCPMC1698767
OpenAlexW2056860545

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.