Evidence map›Paper›PMID 20852067›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Pancreatic stellate cells produce acetylcholine and may play a role in pancreatic exocrine secretion.

Phoebe A Phillips, Lu Yang, Arthur Shulkes, Alain Vonlaufen, Anne Poljak, Sonia Bustamante, Alessandra Warren, Zhihong Xu, Michael Guilhaus, Romano Pirola and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

57 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
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  6. Alterations in exocrine pancreatic function after acute pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024
    Review
  7. Article
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  9. Article
  10. Implicating the cholecystokinin B receptor in liver stem cell oncogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  11. Article
  12. Review
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  14. Intraductal botulinum toxin injection suppressed the inflammation in experimental acute pancreatitis.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2022
    Article
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  16. Review
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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

12 authors at 2 institutions in 2 countries.

Phoebe A PhillipsPancreatic Research Group, South Western Sydney Clinical School and School of Medical Sciences/Pathology, University of New South Wales, Sydney 2052, Australia. p.phillips@unsw.edu.au
Lu Yang
Arthur Shulkes
Alain Vonlaufen
Anne Poljak
Sonia Bustamante
Alessandra Warren
Zhihong Xu
Michael Guilhaus
Romano Pirola
Minoti V Apte
Jeremy S Wilson
UNSW Sydney · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pancreatic secretagogue cholecystokinin (CCK) is widely thought to stimulate enzyme secretion by acinar cells indirectly via activation of the vagus nerve. We postulate an alternative pathway for CCK-induced pancreatic secretion. We hypothesize that neurally related pancreatic stellate cells (PSCs; located in close proximity to the basolateral aspect of acinar cells) play a regulatory role in pancreatic secretion by serving as an intermediate target for CCK and secreting the neurotransmitter acetylcholine (ACh), which, in turn, stimulates acinar enzyme secretion. To determine whether PSCs (i) exhibit CCK-dependent ACh secretion and (ii) influence acinar enzyme secretion, primary cultures of human and rat PSCs were used. Immunoblotting and/or immunofluorescence was used to detect choline acetyltransferase (ACh synthesizing enzyme), vesicular ACh transporter (VAChT), synaptophysin, and CCK receptors 1 and 2. Synaptic-like vesicles in PSCs were identified by EM. ACh secretion by PSCs exposed to 20 pM CCK was measured by LC-MS/MS. Amylase secretion by acini [pretreated with and without the muscarinic receptor antagonist atropine (10 μM) and cocultured with PSCs] was measured by colorimetry. PSCs express ACh synthesizing enzyme, VAChT, synaptophysin, and CCK receptors; exhibit CCK-dependent ACh secretion; and stimulate amylase secretion by acini, which is blocked by atropine. In conclusion, PSCs express the essential elements for ACh synthesis and secretion. CCK stimulates ACh secretion by PSCs, which, in turn, induces amylase secretion by acini. Therefore, PSCs may represent a previously unrecognized intrapancreatic pathway regulating CCK-induced pancreatic exocrine secretion.

Indexed as

Pancreas, ExocrineAcetylcholineAmylasesAnimalsCells, CulturedCholecystokininCholine O-AcetyltransferaseCoculture TechniquesCytoplasmic VesiclesHumansRatsReceptors, CholecystokininSynaptophysinVesicular Acetylcholine Transport ProteinsAcetylcholineAmylasesCholecystokininCholine O-AcetyltransferaseReceptors, CholecystokininSynaptophysinVesicular Acetylcholine Transport Proteins

Identifiers

PMID20852067
PMCPMC2951425
OpenAlexW2131274872

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.