Evidence map›Paper›PMID 20534813›Full record

ArticleMolecular biology of the cell2010

Acid activation of Trpv1 leads to an up-regulation of calcitonin gene-related peptide expression in dorsal root ganglion neurons via the CaMK-CREB cascade: a potential mechanism of inflammatory pain.

Masako Nakanishi, Kenji Hata, Tomotaka Nagayama, Teruhisa Sakurai, Toshihiko Nishisho, Hiroki Wakabayashi, Toru Hiraga, Shigeyuki Ebisu, Toshiyuki Yoneda

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. CaCells · 2021
    Review
  17. 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

9 authors at 4 institutions in 1 country.

Masako NakanishiDepartment of Molecular and Cellular Biology, Osaka University Graduate School of Dentistry, Suita, Osaka, 565-0871, Japan.
Kenji Hata
Tomotaka Nagayama
Teruhisa Sakurai
Toshihiko Nishisho
Hiroki Wakabayashi
Toru Hiraga
Shigeyuki Ebisu
Toshiyuki Yoneda
Osaka University · JPKihoku hospital · JPMatsumoto Dental University · JPMie University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased production of calcitonin gene-related peptide (CGRP) in sensory neurons is implicated in inflammatory pain. The inflammatory site is acidic due to proton release from infiltrating inflammatory cells. Acid activation of peripheral nociceptors relays pain signals to the CNS. Here, we examined whether acid activated the transient receptor potential vanilloid subtype 1 (Trpv1), a widely recognized acid-sensing nociceptor and subsequently increased CGRP expression. Chemically induced inflammation was associated with thermal hyperalgesia and increased CGRP expression in dorsal root ganglion (DRG) in rats. In organ cultures of DRG, acid (pH 5.5) elevated CGRP expression and the selective Trpv1 antagonist 5'-Iodoresiniferatoxin decreased it. Trpv1-deficient DRG showed reduced CGRP increase by acid. Of note, many of CGRP/Trpv1-positive DRG neurons exhibited the phosphorylation of cAMP response element-binding protein (CREB), a nociceptive transcription factor. Knockdown of CREB by small interfering RNA or a dominant-negative form of CREB diminished acid-elevated CGRP expression. Acid elevated the transcriptional activity of CREB, which in turn stimulated CGRP gene promoter activity. These effects were inhibited by a Ca(2+)/calmodulin-dependent protein kinase (CaMK) inhibitor KN-93. In conclusion, our results suggest that inflammatory acidic environments activate Trpv1, leading to an up-regulation of CGRP expression via CaMK-CREB cascade, a series of events that may be associated with inflammatory pain.

Indexed as

AnimalsCalcitonin Gene-Related PeptideCalcium-Calmodulin-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinGanglia, SpinalInflammationIon Channel GatingMiceNeuronsPainPhosphorylationProtonsRatsRNA, MessengerTime FactorsTranscription, GeneticCalcitonin Gene-Related PeptideCalcium-Calmodulin-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinProtonsRNA, MessengerTRPV1 receptorTRPV Cation Channels

Identifiers

PMID20534813
PMCPMC2912344
OpenAlexW2128690456

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.