Evidence map›Paper›PMID 19074643›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009

P2Y receptors mediate Ca2+ signaling in duodenocytes and contribute to duodenal mucosal bicarbonate secretion.

Xiao Dong, Eric James Smoll, Kwang Hyun Ko, Jonathan Lee, Jimmy Yip Chow, Ho Dong Kim, Paul A Insel, Hui Dong

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Distribution of P2Y and P2X purinergic receptor expression within the intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  3. Review
  4. Article
  5. The inhibitory role of purinergic P2Y receptor on MgThe journal of physiological sciences : JPS · 2019
    Article
  6. P2YPurinergic signalling · 2018
    Article
  7. Review
  8. Article
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  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Coupling of P2Y receptors to G proteins and other signaling pathways.Wiley interdisciplinary reviews. Membrane transport and signaling
    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

8 authors at 1 institution in 1 country.

Xiao DongDepartment of Medicine, University of California, La Jolla, CA 92093, USA.
Eric James Smoll
Kwang Hyun Ko
Jonathan Lee
Jimmy Yip Chow
Ho Dong Kim
Paul A Insel
Hui Dong
University of California, San Diego · US

Funding

The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
Adrenergic and Purinergic Regulation of Target CellsR01GM066232 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI INSEL, PAUL A · 2004 to 2010
$1.9M
Mechanisms on the Regulation of PTEN Expression by TGF-BetaK01DK073090 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHOW, YIP · 2006 to 2010
$543k
NIDDK NIH HHS DK073090NIDDK NIH HHS DK-080506NIGMS NIH HHS GM 66232
6 · The paper itself

Abstract

Since little is known about the role of P2Y receptors (purinoceptors) in duodenal mucosal bicarbonate secretion (DMBS), we sought to investigate the expression and function of these receptors in duodenal epithelium. Expression of P2Y(2) receptors was detected by RT-PCR in mouse duodenal epithelium and SCBN cells, a duodenal epithelial cell line. UTP, a P2Y(2)-receptor agonist, but not ADP (10 microM), significantly induced murine duodenal short-circuit current and DMBS in vitro; these responses were abolished by suramin (300 microM), a P2Y-receptor antagonist, or 2-aminoethoxydiphenyl borate (2-APB; 100 microM), a store-operated channel blocker. Mucosal or serosal addition of UTP induced a comparable DMBS in wild-type mice, but markedly impaired response occurred in P2Y(2) knockout mice. Acid-stimulated DMBS in vivo was significantly inhibited by suramin (1 mM) or PPADS (30 microM). Both ATP and UTP, but not ADP (1 microM), raised cytoplasmic-free Ca(2+) concentrations ([Ca(2+)](cyt)) with similar potencies in SCBN cells. ATP-induced [Ca(2+)](cyt) was attenuated by U-73122 (10 microM), La(3+) (30 microM), or 2-APB (10 microM), but was not significantly affected by nifedipine (10 microM). UTP (1 microM) induced a [Ca(2+)](cyt) transient in Ca(2+)-free solutions, and restoration of external Ca(2+) (2 mM) raised [Ca(2+)](cyt) due to capacitative Ca(2+) entry. La(3+) (30 microM), SK&F96365 (30 microM), and 2-APB (10 microM) inhibited UTP-induced Ca(2+) entry by 92, 87, and 94%, respectively. Taken together, our results imply that activation of P2Y(2) receptors enhances DMBS via elevation of [Ca(2+)](cyt) that likely results from an initial increase in intracellular Ca(2+) release followed by extracellular Ca(2+) entry via store-operated channel.

Indexed as

Calcium SignalingAdenosine DiphosphateAminoquinolinesAnimalsBicarbonatesBoron CompoundsCalcium Channel BlockersCell LineDogsDuodenumEpithelial CellsEstrenesFemaleHydrogen-Ion ConcentrationIntestinal MucosaIntestinal Secretions1-(2-methylphenyl)-4-methylamino-6-methyl-2,3-dihydropyrrolo(3,2-c)quinoline1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione2-aminoethoxydiphenyl borateAdenosine DiphosphateAminoquinolinesBicarbonatesBoron CompoundsCalcium Channel BlockersEstrenesNifedipineP2ry2 protein, mousePurinergic P2 Receptor AntagonistsPyridoxal Phosphatepyridoxal phosphate-6-azophenyl-2',4'-disulfonic acidPyrrolidinonesReceptors, Purinergic P2Receptors, Purinergic P2Y2SuraminUridine Triphosphate

Identifiers

PMID19074643
PMCPMC2643905
OpenAlexW2121294008

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.