Evidence map›Paper›PMID 17135311›Full record

ArticleGut2007

Suppression of transforming growth factor beta signalling aborts caerulein induced pancreatitis and eliminates restricted stimulation at high caerulein concentrations.

Stefan Wildi, Jörg Kleeff, Julia Mayerle, Arthur Zimmermann, Erwin P Böttinger, Lalage Wakefield, Markus W Büchler, Helmut Friess, Murray Korc

Abstract read
In one paragraph

Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

60 citing papers in PubMed, 101 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. CD177Cellular and molecular life sciences : CMLS · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

9 authors at 5 institutions in 3 countries.

Stefan WildiDepartment of Medicine and Pharmacology & Toxicology, Dartmouth Medical School, Hanover, New Hampshire, USA.
Jörg Kleeff
Julia Mayerle
Arthur Zimmermann
Erwin P Böttinger
Lalage Wakefield
Markus W Büchler
Helmut Friess
Murray Korc
Heidelberg University · DEDartmouth–Hitchcock Medical Center · USIcahn School of Medicine at Mount Sinai · USNational Cancer Institute · USUniversity of Bern · CH

Funding

Novel aspects of Epithelial-Mesenchymal Transition(EMT)in pancreatic cancerR01CA075059 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KORC, MURRAY · 1997 to 2018
$4.3M
CYTOKINE SIGNALING IN RENAL FIBROSISR01DK056077 · NIDDK · YESHIVA UNIVERSITY · PI BOTTINGER, ERWIN P. · 1999 to 2009
$3.2M
Genetic Programming in Progressive Renal DiseaseR01DK060043 · NIDDK · YESHIVA UNIVERSITY · PI BOTTINGER, ERWIN P. · 2001 to 2010
$2.9M
Dysregulation of TGF Beta Action Pancreatic CancerR37CA075059 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KORC, MURRAY · 2008 to 2012
$2.2M
NCI NIH HHS CA-75059NIDDK NIH HHS R01 DK056077NIDDK NIH HHS R01 DK060043
6 · The paper itself

Abstract

backgroundTransforming growth factors betas (TGF-betas) are implicated in pancreatic tissue repair but their role in acute pancreatitis is not known. To determine whether endogenous TGF-betas modulate the course of caerulein induced acute pancreatitis, caerulein was administered to wild-type (FVB-/-) and transgenic mice that are heterozygous (FVB+/-) for expression of a dominant negative type II TGF-beta receptor.

methodsAfter 7 hourly supramaximal injections of caerulein, the pancreas was evaluated histologically and serum was assayed for amylase and lipase levels. Next, the effects of caerulein on amylase secretion were determined in mouse pancreatic acini, and cholecystokinin (CCK) receptor expression was assessed.

resultsThe normal mouse pancreas was devoid of inflammatory cells whereas the pancreas from transgenic mice contained lymphocytic infiltrates. Caerulein injection in wild-type mice resulted in 6- and 36-fold increases in serum amylase and lipase levels, respectively, increased serum trypsinogen activation peptide (TAP) levels, gross oedema and a marked inflammatory response in the pancreas that consisted mainly of neutrophils and macrophages. By contrast, FVB+/- mice exhibited minimal alterations in response to caerulein with attenuated neutrophil-macrophage infiltrates. Moreover, acini from FVB+/- mice did not exhibit restricted stimulation at high caerulein concentrations, even though CCK receptor mRNA levels were not decreased.

conclusionOur findings indicate that a functional TGF-beta signalling pathway may be required for caerulein to induce acute pancreatitis and for the CCK receptor to induce acinar cell damage at high ligand concentrations. Our results also support the concept that restricted stimulation at high caerulein concentrations contributes to the ability of caerulein to induce acute pancreatitis.

Indexed as

Acute DiseaseAmylasesAnimalsBlotting, NorthernCeruletideEdemaLigandsLipaseMiceMice, TransgenicOligopeptidesPancreatic DiseasesPancreatitisReceptors, CholecystokininSeverity of Illness IndexSignal TransductionAmylasesCeruletideLigandsLipaseOligopeptidesReceptors, CholecystokininTransforming Growth Factor betatrypsinogen activation peptide

Identifiers

PMID17135311
PMCPMC1942167
OpenAlexW2284090748

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.