Evidence map›Paper›PMID 12574409›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Stimulation of the calcitonin gene-related peptide enhancer by mitogen-activated protein kinases and repression by an antimigraine drug in trigeminal ganglia neurons.

Paul L Durham, Andrew F Russo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Review
  7. Article
  8. Article
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  10. Article
  11. Cross-talk signaling in the trigeminal ganglion: role of neuropeptides and other mediators.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  12. Article
  13. Review
  14. Review
  15. Current understanding of trigeminal ganglion structure and function in headache.Cephalalgia : an international journal of headache · 2019
    Review
  16. Anti-CGRP in cluster headache therapy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Review
  17. Sumatriptan ameliorates renal injury induced by cisplatin in mice.Iranian journal of basic medical sciences · 2019
    Article
  18. Article
  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

2 authors at 1 institution in 1 country.

Paul L DurhamDepartment of Physiology and Biophysics, University of Iowa, Iowa City, Iowa 52242, USA. pauldurham@smsu.edu
Andrew F Russo
University of Iowa · US

Funding

VASOPRESSIN IN CARDIOVASCULAR REGULATIONP01HL014388 · NHLBI · UNIVERSITY OF IOWA · PI SANFORD, L PHILLIP · 1985 to 2018
$40.3M
SITE SPECIFIC ANTIINSULIN RECEPTOR ANTIBODIESP30DK025295 · NIDDK · UNIVERSITY OF IOWA · PI BAR, ROBERT S · 1986 to 2002
$2.6M
NEURONAL CONTROL OF CGRP GENE EXPRESSIONR01HD025969 · NICHD · UNIVERSITY OF IOWA · PI RUSSO, ANDREW F · 1991 to 2003
$999k
NHLBI NIH HHS HL 14388NHLBI NIH HHS P01 HL014388NICHD NIH HHS HD 25969NICHD NIH HHS R01 HD025969NIDDK NIH HHS DK 25295
6 · The paper itself

Abstract

Calcitonin gene-related peptide (CGRP) is involved in the underlying pathophysiology of all vascular headaches, including migraines. Elevated levels of CGRP during migraine are restored to normal coincident with headache relief after treatment with the antimigraine drug sumatriptan. We have used primary cultures of trigeminal neurons under conditions simulating migraine pathology and therapy to study the mechanisms controlling the CGRP promoter. Using reporter genes in transient transfection assays, we demonstrate that an 18 bp enhancer containing a helix-loop-helix element is both necessary and sufficient for full promoter activity. NGF treatment and cotransfection with an upstream activator of the extracellular signal-regulated MAP kinases (MAPKs) activated the enhancer. Treatment with sumatriptan repressed NGF- and MAPK-stimulated CGRP promoter activity. Repression was also observed using a synthetic MAPK-responsive reporter gene. Sumatriptan regulation of CGRP gene expression did not couple to a G(i)/G(o) pathway, but rather caused a prolonged increase in intracellular calcium. The importance of the prolonged calcium signal in repression of MAPK activity was demonstrated by using the ionophore ionomycin to mimic sumatriptan action. We propose that activation of MAPK pathways may increase CGRP gene expression during migraine, and that sumatriptan can diametrically oppose that activation via a prolonged elevation of intracellular calcium.

Indexed as

AnimalsCalcitonin Gene-Related PeptideCalciumCells, CulturedEnhancer Elements, GeneticGene Expression RegulationGenes, ReporterHelix-Turn-Helix MotifsIntracellular FluidIonophoresMigraine DisordersMitogen-Activated Protein KinasesNerve Growth FactorNeuronsPertussis ToxinPromoter Regions, GeneticCalcitonin Gene-Related PeptideCalciumIonophoresMitogen-Activated Protein KinasesNerve Growth FactorPertussis ToxinSumatriptanVasoconstrictor Agents

Identifiers

PMID12574409
PMCPMC6741928
OpenAlexW2124796000

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.