Evidence map›Paper›PMID 20969730›Full record

ArticleActa physiologica (Oxford, England)2011

Expression of acid-sensing ion channels in intestinal epithelial cells and their role in the regulation of duodenal mucosal bicarbonate secretion.

X Dong, K H Ko, J Chow, B Tuo, K E Barrett, H Dong

Open access · greenAbstract read
In one paragraph

Article in Acta physiologica (Oxford, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Acid-Sensing Ion Channels and Mechanosensation.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. The inhibitory role of purinergic P2Y receptor on MgThe journal of physiological sciences : JPS · 2019
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. CaOncotarget · 2017
    Review
  16. Article
  17. Article
  18. Review
  19. ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012
    Review
  20. 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

6 authors at 2 institutions in 3 countries.

X DongDepartment of Medicine, University of California, San Diego, USA.
K H Ko
J Chow
B Tuo
K E Barrett
H Dong
University of California San Diego · USAffiliated Hospital of Zunyi Medical College · CN

Funding

The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
NIDDK NIH HHS DK-080506NIDDK NIH HHS R24 DK080506
6 · The paper itself

Abstract

aimsAs little is currently known about acid-sensing ion channels (ASICs) in intestinal epithelial cells, the aims of the present study were to investigate the expression and function of ASICs in intestinal epithelial cells, particularly their physiological role in the acid-stimulated duodenal mucosal bicarbonate secretion (DMBS).

methodsRT-PCR and digital Ca²(+) imaging were used to determine the expression and function of ASICs in HT29 cells and SCBN cells, intestinal epithelial crypt cell lines. The acid-stimulated DMBS was measured in C57 black mice in vivo to study the role of ASICs in this physiological process.

resultsASIC1a mRNA expression was detected in the duodenal mucosa stripped from mice and epithelial cell lines, in which cytoplasmic free Ca²(+) ([Ca²(+) ](cyt)) in response to extracellular acidosis was also increased. In Ca²(+) -containing solutions, acidosis (pH 6.0-5.0) raised [Ca²(+) ](cyt) in both HT29 cells and SCBN cells in a similar pH-dependent manner. Acidosis-induced increase in [Ca²(+) ](cyt) was markedly inhibited by amiloride (an ASICs blocker), SK&F96365 (a blocker for non-selective cation channels), or in Ca²(+) -free solutions; but was abolished by amiloride in Ca²(+) -free solutions. However, acidosis-induced increase in [Ca²(+) ](cyt) was slightly affected by U73122 (a PLC inhibitor), or nifedipine (a voltage-gated Ca²(+) channel blocker). After acidosis raised [Ca²(+) ](cyt) , stimulation of purinergic receptors with ATP further increased [Ca²(+) ](cyt) , but acidosis-induced increase in [Ca²(+) ](cyt) was not altered by suramin. Moreover, acid-stimulated murine DMBS was significantly attenuated by amiloride.

conclusionTherefore, ASICs are functionally expressed in intestinal epithelial cells, and may play a role in acid-stimulated DMBS through a Ca²(+) signalling pathway.

Indexed as

Acid Sensing Ion ChannelsAmilorideAnimalsBicarbonatesCalciumCell LineDuodenumEpithelial CellsHumansHydrogen-Ion ConcentrationIntestinal MucosaMiceMice, Inbred C57BLNerve Tissue ProteinsSignal TransductionSodium Channel BlockersAcid Sensing Ion ChannelsAmilorideASIC1 protein, humanASIC1 protein, mouseBicarbonatesCalciumNerve Tissue ProteinsSodium Channel BlockersSodium ChannelsSuramin

Identifiers

PMID20969730
PMCPMC4095866
OpenAlexW2131753272

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Registered trials

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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.