Evidence map›Paper›PMID 17114010›Full record

ArticleJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract2006

Pancreatic regeneration in chronic pancreatitis requires activation of the notch signaling pathway.

Yun Su, Peter Büchler, Amiq Gazdhar, Nathalia Giese, Howard A Reber, Oscar J Hines, Thomas Giese, Markus W Büchler, Helmut Friess

Abstract read
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Article in Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Notch Signaling in Pancreatic Development.International journal of molecular sciences · 2015
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Ligand-dependent Notch signaling is involved in tumor initiation and tumor maintenance in pancreatic cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Article
  14. Article
  15. Article
  16. 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 4 institutions in 3 countries.

Yun SuDepartment of General Surgery, University of Heidelberg, Heidelberg, Germany.
Peter Büchler
Amiq Gazdhar
Nathalia Giese
Howard A Reber
Oscar J Hines
Thomas Giese
Markus W Büchler
Helmut Friess
Heidelberg University · DEZhongda Hospital Southeast University · CNUniversity of California, Los Angeles · USUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pancreatitis as an inflammatory process characterized by morphological changes, pancreatic dysfunction, and pain. During pancreatic injury and repair the Notch signaling pathway is reinstated. The current study analyzed this pathway in chronic pancreatitis and characterized its influence on fibrogenesis. Real-time quantitative PCR and immunohistochemistry were used for expression studies. Notch activation was determined by a specific luciferase-HES-1-reporter gene constructs. Cells were stimulated with alcohol, glucose, bile acids, and steroids. Notch-2, -3, and -4 mRNA, were overexpressed in chronic pancreatitis specimens. The ligands Jagged-1, -2, and Delta-1 were highly overexpressed. Jagged-1 and Notch receptors were observed in nerves, regenerating exocrine cells, and endocrine cells. Delta staining was present in ductal but not in acinus cells and not in nerves. Activation of Notch signaling was detectable upon cell stimulation with glucose, steroids, and bile acids. High glucose levels were further associated with increased collagen-I production. The Notch pathway is reactivated during chronic pancreatitis. Among the stimuli activating the Notch pathway are steroids, high glucose levels, and bile acids. These findings suggest a possible role of the Notch pathway during pancreatic regeneration since Jagged-1 inhibits inducible collagen-1 production, suggesting a new mechanism of tissue repair in this disease.

Indexed as

RegenerationSignal TransductionAnimalsBlotting, NorthernBlotting, WesternCalcium-Binding ProteinsCells, CulturedCollagen Type IFibroblastsFibrosisGene ExpressionHumansIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsJagged-1 ProteinLigandsCalcium-Binding ProteinsCollagen Type Idelta proteinIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsJAG1 protein, humanJag1 protein, mouseJagged-1 ProteinLigandsLuciferases, RenillaMembrane ProteinsReceptors, NotchRNASerrate-Jagged Proteins

Identifiers

PMID17114010
OpenAlexW1971784499

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.