Evidence map›Paper›PMID 21737902›Full record

ArticleJOP : Journal of the pancreas2011

Substance P and calcitonin gene related peptide mediate pain in chronic pancreatitis and their expression is driven by nerve growth factor.

LianSheng Liu, Mohan Shenoy, Pankaj Jay Pasricha

Open access · greenAbstract read
In one paragraph

Article in JOP : Journal of the pancreas, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  7. Review
  8. Serum biomarkers for chronic pancreatitis pain patterns.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2021
    Article
  9. Pancreas-Brain Crosstalk.Frontiers in neuroanatomy · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Unraveling the mystery of pain in chronic pancreatitis.Nature reviews. Gastroenterology & hepatology · 2012
    Review
  20. Mechanism, assessment and management of pain in chronic pancreatitis: Recommendations of a multidisciplinary study group.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
    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

3 authors at 1 institution in 1 country.

LianSheng LiuDivision of Gastroenterology and Hepatology, Stanford University Medical Center, Stanford, CA, USA.
Mohan Shenoy
Pankaj Jay Pasricha
Stanford University · US

Funding

Proteomics/GenomicsP30DK056339 · NIDDK · STANFORD UNIVERSITY · PI GREENBERG, HARRY BERNARD · 2001 to 2010
$10.4M
Molecular Mechanisms of Pain in Chronic PancreatitisR01DK073558 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI PASRICHA, PANKAJ J · 2007 to 2015
$2.7M
NIDDK NIH HHS P30 DK056339NIDDK NIH HHS P30 DK56339NIDDK NIH HHS R01 DK073558
6 · The paper itself

Abstract

contextCalcitonin gene-related peptide (CGRP), substance P and nerve growth factor play an important role in inflammatory pain in various somatic pain models but their role in chronic pancreatitis has not been well studied.

objectivesThe aim of this study was to investigate the effects of intrathecal administration of calcitonin gene-related peptide antagonist and substance P receptor antagonist on pain behavior in a rat model of chronic pancreatitis and to determine whether nerve growth factor drives the up-regulation of expression of these neuropeptides in sensory neurons.

methodsPancreatitis was induced by retrograde infusion of trinitobenzene sulfonic acid into the pancreatic duct of adult rats. Three weeks post infusion continuous intrathecal infusion of the calcitonin gene-related peptide antagonist alpha CGRP8-37 or neurokinin-1 receptor antagonist CP-96345 or its inactive enantiomer CP-96344 was administered for seven days. The effects of treatment on pancreatic hyperalgesia were assessed by sensitivity of the abdominal wall to von Frey filament probing as well as by the nocifensive response to electrical stimulation of the pancreas. In a separate experiment chronic pancreatitis was induced and pancreas specific dorsal root ganglion neurons labeled with DiI were assessed for calcitonin gene-related peptide and substance P immunoreactivity.

resultsIntrathecal infusion of calcitonin gene-related peptide and neurokinin-1 receptor antagonists significantly attenuated behavioral pain responses in rats with chronic pancreatitis. Further, treatment of chronic pancreatitis rats with nerve growth factor antibody significantly reduced pancreas specific neurons expressing calcitonin gene-related peptide and substance P in thoracic dorsal root ganglion.

conclusionsCalcitonin gene-related peptide and substance P mediate pancreatic hyperalgesia in chronic pancreatitis and nerve growth factor in turn sustains the up-regulation of these neuropeptides in pancreatic sensory neurons.

Indexed as

AnimalsBiphenyl CompoundsCalcitonin Gene-Related PeptideDrug Evaluation, PreclinicalGene Expression RegulationInjections, SpinalMaleNerve Growth FactorNociceptive PainPainPain MeasurementPancreatitis, ChronicPeptide FragmentsRatsRats, Sprague-DawleySubstance PBiphenyl CompoundsCalcitonin Gene-Related Peptidecalcitonin gene-related peptide (8-37)CP 96345Nerve Growth FactorPeptide FragmentsSubstance P

Identifiers

PMID21737902
PMCPMC4090212
OpenAlexW2158267870

What OpenQuestion holds

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LicenceTDM
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.