Evidence map›Paper›PMID 24086766›Full record

ArticlePloS one2013

Reactive oxygen species are required for 5-HT-induced transactivation of neuronal platelet-derived growth factor and TrkB receptors, but not for ERK1/2 activation.

Jeff S Kruk, Maryam S Vasefi, John J Heikkila, Michael A Beazely

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Preoperative SSRI use increases perioperative transfusion need in patients undergoing surgical procedures on the hip joint.European journal of orthopaedic surgery & traumatology : orthopedie traumatologie · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. The Chronic Treatment With 5-HTNeurochemical research · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. ROS and ROS-Mediated Cellular Signaling.Oxidative medicine and cellular longevity · 2016
    Review
  13. Review
  14. 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

4 authors at 1 institution in 1 country.

Jeff S KrukDepartment of Biology, University of Waterloo, Waterloo, Ontario, Canada.
Maryam S Vasefi
John J Heikkila
Michael A Beazely
University of Waterloo · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High concentrations of reactive oxygen species (ROS) induce cellular damage, however at lower concentrations ROS act as intracellular second messengers. In this study, we demonstrate that serotonin (5-HT) transactivates the platelet-derived growth factor (PDGF) type β receptor as well as the TrkB receptor in neuronal cultures and SH-SY5Y cells, and that the transactivation of both receptors is ROS-dependent. Exogenous application of H₂O₂ induced the phosphorylation of these receptors in a dose-dependent fashion, similar to that observed with 5-HT. However the same concentrations of H₂O₂ failed to increase ERK1/2 phosphorylation. Yet, the NADPH oxidase inhibitors diphenyleneiodonium chloride and apocynin blocked both 5-HT-induced PDGFβ receptor phosphorylation and ERK1/2 phosphorylation. The increases in PDGFβ receptor and ERK1/2 phosphorylation were also dependent on protein kinase C activity, likely acting upstream of NADPH oxidase. Additionally, although the ROS scavenger N-acetyl-l-cysteine abrogated 5-HT-induced PDGFβ and TrkB receptor transactivation, it was unable to prevent 5-HT-induced ERK1/2 phosphorylation. Thus, the divergence point for 5-HT-induced receptor tyrosine kinase (RTK) transactivation and ERK1/2 phosphorylation occurs at the level of NADPH oxidase in this system. The ability of 5-HT to induce the production of ROS resulting in transactivation of both PDGFβ and TrkB receptors may suggest that instead of a single GPCR to single RTK pathway, a less selective, more global RTK response to GPCR activation is occurring.

Indexed as

AnimalsCell Line, TumorEnzyme ActivationHumansMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH OxidasesNeuronsPhosphorylationReactive Oxygen SpeciesReceptor, Platelet-Derived Growth Factor betaReceptor, trkBSerotoninTranscriptional ActivationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH OxidasesReactive Oxygen SpeciesReceptor, Platelet-Derived Growth Factor betaReceptor, trkBSerotonin

Identifiers

PMID24086766
PMCPMC3785432
OpenAlexW2011421397

What OpenQuestion holds

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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.