Evidence map›Paper›PMID 30933959›Full record

ArticlePain2019

Platelet-derived growth factor activates nociceptive neurons by inhibiting M-current and contributes to inflammatory pain.

Omer Barkai, Stephanie Puig, Shaya Lev, Ben Title, Ben Katz, Luba Eli-Berchoer, Howard B Gutstein, Alexander M Binshtok

Open access · hybridAbstract read
In one paragraph

Article in Pain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
3.0field-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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Platelets Enter the Itch Circuit.Research (Washington, D.C.) · 2026
    Article
  8. Article
  9. Article
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  11. Observational
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  13. c-Kit Receptor Maintains Sensory Axon Innervation of the Skin through Src Family Kinases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
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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

8 authors at 2 institutions in 2 countries.

Omer BarkaiDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Stephanie PuigDepartment of Anesthesiology, University of Pittsburgh, Pittsburgh, PA, United States.
Shaya LevDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Ben TitleDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Ben KatzDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Luba Eli-BerchoerThe Institute of Dental Sciences, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Howard B GutsteinDepartment of Anesthesiology, University of Pittsburgh, Pittsburgh, PA, United States.
Alexander M BinshtokDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Hebrew University of Jerusalem · ILUniversity of Pittsburgh · US

Funding

The role of RTK signaling in opioid toleranceR01DA036680 · NIDA · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI GUTSTEIN, HOWARD B · 2014 to 2018
$1.8M
NIDA NIH HHS R01 DA036680
6 · The paper itself

Abstract

Endogenous inflammatory mediators contribute to the pathogenesis of pain by acting on nociceptors, specialized sensory neurons that detect noxious stimuli. Here, we describe a new factor mediating inflammatory pain. We show that platelet-derived growth factor (PDGF)-BB applied in vitro causes repetitive firing of dissociated nociceptor-like rat dorsal root ganglion neurons and decreased their threshold for action potential generation. Injection of PDGF-BB into the paw produced nocifensive behavior in rats and led to thermal and mechanical pain hypersensitivity. We further detailed the biophysical mechanisms of these PDGF-BB effects and show that PDGF receptor-induced inhibition of nociceptive M-current underlies PDGF-BB-mediated nociceptive hyperexcitability. Moreover, in vivo sequestration of PDGF or inhibition of the PDGF receptor attenuates acute formalin-induced inflammatory pain. Our discovery of a new pain-facilitating proinflammatory mediator, which by inhibiting M-current activates nociceptive neurons and thus contributes to inflammatory pain, improves our understanding of inflammatory pain pathophysiology and may have important clinical implications for pain treatment.

Indexed as

Action PotentialsAnimalsGanglia, SpinalHyperalgesiaInflammationMaleNociceptorsPainPain MeasurementPlatelet-Derived Growth FactorRats, Sprague-DawleySensory Receptor CellsPlatelet-Derived Growth Factor

Identifiers

PMID30933959
PMCPMC6553959
OpenAlexW2919648530

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.