Evidence map›Paper›PMID 23448290›Full record

ArticleMolecular pain2013

Involvement of TRPA1 activation in acute pain induced by cadmium in mice.

Saeko Miura, Kenji Takahashi, Toshiaki Imagawa, Kunitoshi Uchida, Shigeru Saito, Makoto Tominaga, Toshio Ohta

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Inflammation-the role of TRPA1 channel.Frontiers in physiology · 2023
    Review
  5. Research progress on mechanism of Chinese Kaiqiao herbs in management of neuropathic pain.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
  6. Review
  7. Article
  8. TRPA1 Expression and Pathophysiology in Immune Cells.International journal of molecular sciences · 2021
    Review
  9. Using FluoZin-3 and fura-2 to monitor acute accumulation of free intracellular CdBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2019
    Article
  10. Article
  11. Cadmium-induced neurotoxicity: still much ado.Neural regeneration research · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
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

7 authors at 4 institutions in 1 country.

Saeko MiuraDepartment of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, Tottori 680-8553, Japan.
Kenji Takahashi
Toshiaki Imagawa
Kunitoshi Uchida
Shigeru Saito
Makoto Tominaga
Toshio Ohta
Tottori University · JPNational Institutes of Natural Sciences · JPHokkaido University · JPNational Institute for Physiological Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCadmium (Cd) is an environmental pollutant and acute exposure to it causes symptoms related to pain and inflammation in the airway and gastrointestinal tract, but the underlying mechanisms are still unclear. TRPA1 is a nonselective cation channel expressed in sensory neurons and acts as a nociceptive receptor. Some metal ions such as Ca, Mg, Ba and Zn are reported to modulate TRPA1 channel activity. In the present study, we investigated the effect of Cd on cultured mouse dorsal root ganglion neurons and a heterologous expression system to analyze the effect of Cd at the molecular level. In addition, we examined whether Cd caused acute pain in vivo.

resultsIn wild-type mouse sensory neurons, Cd evoked an elevation of the intracellular Ca concentration ([Ca2+]i) that was inhibited by external Ca removal and TRPA1 blockers. Most of the Cd-sensitive neurons were also sensitive to cinnamaldehyde (a TRPA1 agonist) and [Ca2+]i responses to Cd were absent in TRPA1(-/-) mouse neurons. Heterologous expression of TRPA1 mutant channels that were less sensitive to Zn showed attenuation of Cd sensitivity. Intracellular Cd imaging revealed that Cd entered sensory neurons through TRPA1. The stimulatory effects of Cd were confirmed in TRPA1-expressing rat pancreatic cancer cells (RIN-14B). Intraplantar injection of Cd induced pain-related behaviors that were largely attenuated in TRPA1(-/-) mice.

conclusionsCd excites sensory neurons via activation of TRPA1 and causes acute pain, the mechanism of which may be similar to that of Zn. The present results indicate that TRPA1 is involved in the nociceptive or inflammatory effects of Cd.

Indexed as

Acute PainAnimalsCadmiumCalciumCell Line, TumorFemaleGanglia, SpinalHumansIon Channel GatingMaleMiceMice, Inbred C57BLMutant ProteinsPancreatic NeoplasmsRatsSensory Receptor CellsCadmiumCalciumMutant ProteinsTransient Receptor Potential ChannelsTRPA1 Cation ChannelTrpa1 protein, mouseZinc

Identifiers

PMID23448290
PMCPMC3599231
OpenAlexW2125276639

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.