Evidence map›Paper›PMID 28348394›Full record

ArticleScientific reports2017

The G2A receptor (GPR132) contributes to oxaliplatin-induced mechanical pain hypersensitivity.

Stephan W Hohmann, Carlo Angioni, Sorin Tunaru, Seungkyu Lee, Clifford J Woolf, Stefan Offermanns, Gerd Geisslinger, Klaus Scholich, Marco Sisignano

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

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  11. Targeting sensory neuron GPCRs for peripheral neuropathic pain.Trends in pharmacological sciences · 2023
    Review
  12. Antinociceptive Effect ofLife (Basel, Switzerland) · 2023
    Article
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  15. Article
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  19. Review
  20. Oxaliplatin Causes Transient Changes in TRPM8 Channel Activity.International journal of molecular sciences · 2021
    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 3 institutions in 2 countries.

Stephan W HohmannInstitute of Clinical Pharmacology, pharmazentrum frankfurt/ZAFES, University Hospital, Goethe-University, D-60590, Frankfurt am Main, Germany.
Carlo AngioniInstitute of Clinical Pharmacology, pharmazentrum frankfurt/ZAFES, University Hospital, Goethe-University, D-60590, Frankfurt am Main, Germany.
Sorin TunaruDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Seungkyu LeeF. M. Kirby Neurobiology Center, Children's Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, MA, 02115, USA.ORCID 0000-0002-1929-3320
Clifford J WoolfF. M. Kirby Neurobiology Center, Children's Hospital Boston, and Department of Neurobiology, Harvard Medical School, Boston, MA, 02115, USA.
Stefan OffermannsDepartment of Pharmacology, Max-Planck-Institute for Heart and Lung Research, 61231, Bad Nauheim, Germany.
Gerd GeisslingerInstitute of Clinical Pharmacology, pharmazentrum frankfurt/ZAFES, University Hospital, Goethe-University, D-60590, Frankfurt am Main, Germany.
Klaus ScholichInstitute of Clinical Pharmacology, pharmazentrum frankfurt/ZAFES, University Hospital, Goethe-University, D-60590, Frankfurt am Main, Germany.
Marco SisignanoInstitute of Clinical Pharmacology, pharmazentrum frankfurt/ZAFES, University Hospital, Goethe-University, D-60590, Frankfurt am Main, Germany. marco.sisignano@med.uni-frankfurt.de.ORCID 0000-0002-7581-0951
Goethe University Frankfurt · DEBoston Children's Hospital · USMax Planck Institute for Heart and Lung Research · DE

Funding

ALTERED SENSIBILITY FOLLOWING PERIPHERAL NERVE DAMAGER01NS038253 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI WOOLF, CLIFFORD J · 1999 to 2017
$8.2M
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2M
NICHD NIH HHS U54 HD090255NINDS NIH HHS R01 NS038253
6 · The paper itself

Abstract

Chemotherapy-induced peripheral neuropathic pain (CIPN) is a common and severe debilitating side effect of many widely used cytostatics. However, there is no approved pharmacological treatment for CIPN available. Among other substances, oxaliplatin causes CIPN in up to 80% of treated patients. Here, we report the involvement of the G-protein coupled receptor G2A (GPR132) in oxaliplatin-induced neuropathic pain in mice. We found that mice deficient in the G2A-receptor show decreased mechanical hypersensitivity after oxaliplatin treatment. Lipid ligands of G2A were found in increased concentrations in the sciatic nerve and dorsal root ganglia of oxaliplatin treated mice. Calcium imaging and patch-clamp experiments show that G2A activation sensitizes the ligand-gated ion channel TRPV1 in sensory neurons via activation of PKC. Based on these findings, we conclude that targeting G2A may be a promising approach to reduce oxaliplatin-induced TRPV1-sensitization and the hyperexcitability of sensory neurons and thereby to reduce pain in patients treated with this chemotherapeutic agent.

Indexed as

AnimalsCell Cycle ProteinsCyclic AMP-Dependent Protein KinasesEnzyme ActivationGanglia, SpinalHyperalgesiaLinoleic Acids, ConjugatedMice, Inbred C57BLNeuralgiaOrganoplatinum CompoundsOxaliplatinProtein Kinase CReceptors, G-Protein-CoupledSciatic NerveSensory Receptor CellsTRPV Cation Channels9-hydroxy-10,12-octadecadienoic acidCell Cycle ProteinsCyclic AMP-Dependent Protein KinasesG2A receptorLinoleic Acids, ConjugatedOrganoplatinum CompoundsOxaliplatinProtein Kinase CReceptors, G-Protein-CoupledTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID28348394
PMCPMC5428564
OpenAlexW2598458960

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.