Evidence map›Paper›PMID 20843811›Full record

ArticleThe Journal of biological chemistry2010

CCK1 and CCK2 receptors are expressed on pancreatic stellate cells and induce collagen production.

Marc J Berna, Oliver Seiz, Jan Friso Nast, Daniel Benten, Michael Bläker, Johannes Koch, Ansgar W Lohse, Andrea Pace

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Alterations in exocrine pancreatic function after acute pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024
    Review
  10. Article
  11. Article
  12. Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  13. Article
  14. Article
  15. Target-Specific Nanoparticle Polyplex Down-Regulates MutantInternational journal of molecular sciences · 2023
    Article
  16. Review
  17. Article
  18. Article
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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 3 institutions in 1 country.

Marc J BernaUniversitätsklinikum Eppendorf, Medizinische Klinik I, 20246 Hamburg, Germany.
Oliver Seiz
Jan Friso Nast
Daniel Benten
Michael Bläker
Johannes Koch
Ansgar W Lohse
Andrea Pace
Eppendorf (Germany) · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gastrointestinal hormone cholecystokinin (CCK) can induce acute pancreatitis in rodents through its action on acinar cells. Treatment with CCK, in combination with other agents, represents the most commonly used model to induce experimental chronic pancreatitis. Pancreatic stellate cells (PSC) are responsible for pancreatic fibrosis and therefore play a predominant role in the genesis of chronic pancreatitis. However, it is not known whether PSC express CCK receptors. Using real time PCR techniques, we demonstrate that CCK1 and CCK2 receptors are expressed on rat PSC. Interestingly both CCK and gastrin significantly induced type I collagen synthesis. Moreover, both inhibit proliferation. These effects are comparable with TGF-β-stimulated PSC. Furthermore, the natural agonists CCK and gastrin induce activation of pro-fibrogenic pathways Akt, ERK, and Src. Using specific CCK1 and CCK2 receptor (CCK2R) inhibitors, we found that Akt activation is mainly mediated by CCK2R. Akt activation by CCK and gastrin could be inhibited by the PI3K inhibitor wortmannin. Activation of ERK and the downstream target Elk-1 could be inhibited by the MEK inhibitor U0126. These data suggest that CCK and gastrin have direct activating effects on PSC, are able to induce collagen synthesis in these cells, and therefore appear to be important regulators of pancreatic fibrogenesis. Furthermore, similar to TGF-β, both CCK and gastrin inhibit proliferation in PSC.

Indexed as

Gene Expression RegulationAnimalsButadienesCollagenCollagen Type IEnzyme InhibitorsGastrinsMaleNitrilesPancreasPancreatic Stellate CellsRatsRats, Sprague-DawleyReceptor, Cholecystokinin BReceptors, CholecystokininSignal TransductionButadienesCollagenCollagen Type IEnzyme InhibitorsGastrinsNitrilesReceptor, Cholecystokinin BReceptors, CholecystokininTransforming Growth Factor betaU 0126

Identifiers

PMID20843811
PMCPMC2998120
OpenAlexW2088112676

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.