Evidence map›Paper›PMID 23801362›Full record

ArticlePurinergic signalling2013

Changes of the GPR17 receptor, a new target for neurorepair, in neurons and glial cells in patients with traumatic brain injury.

Heike Franke, Chiara Parravicini, Davide Lecca, Elisa R Zanier, Claudia Heine, Kristina Bremicker, Marta Fumagalli, Patrizia Rosa, Luca Longhi, Nino Stocchetti and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Purinergic signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-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

40 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. GPR17 modulates anxiety-like behaviorsActa pharmaceutica Sinica. B · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Involvement of GPR17 in Neuronal Fibre Outgrowth.International journal of molecular sciences · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. The Roles of Orphan G Protein-Coupled Receptors in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021
    Review
  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

13 authors at 5 institutions in 2 countries.

Heike FrankeRudolf Boehm Institute of Pharmacology and Toxicology, University of Leipzig, Leipzig, Germany.
Chiara Parravicini
Davide Lecca
Elisa R Zanier
Claudia Heine
Kristina Bremicker
Marta Fumagalli
Patrizia Rosa
Luca Longhi
Nino Stocchetti
Maria-Grazia De Simoni
Marco Weber
Maria P Abbracchio
University of Milan · ITLeipzig University · DEMario Negri Institute for Pharmacological Research · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITNeuroscience Institute · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unveiling the mechanisms participating in the damage and repair of traumatic brain injury (TBI) is fundamental to develop new therapies. The P2Y-like GPR17 receptor has recently emerged as a sensor of damage and a key actor in lesion remodeling/repair in the rodent brain, but its role in humans is totally unknown. Here, we characterized GPR17 expression in brain specimens from seven intensive care unit TBI patients undergoing neurosurgery for contusion removal and from 28 autoptic TBI cases (and 10 control subjects of matched age and gender) of two university hospitals. In both neurosurgery and autoptic samples, GPR17 expression was strong inside the contused core and progressively declined distally according to a spatio-temporal gradient. Inside and around the core, GPR17 labeled dying neurons, reactive astrocytes, and activated microglia/macrophages. In peri-contused parenchyma, GPR17 decorated oligodendrocyte precursor cells (OPCs) some of which had proliferated, indicating re-myelination attempts. In autoptic cases, GPR17 expression positively correlated with death for intracranial complications and negatively correlated with patients' post-traumatic survival. Data indicate lesion-specific sequential involvement of GPR17 in the (a) death of irreversibly damaged neurons, (b) activation of microglia/macrophages remodeling the lesion, and (c) activation/proliferation of multipotent parenchymal progenitors (both reactive astrocytes and OPCs) starting repair processes. Data validate GPR17 as a target for neurorepair and are particularly relevant to setting up new therapies for TBI patients.

Indexed as

AdultAgedBrain InjuriesFemaleHumansImmunohistochemistryMaleMicroscopy, ConfocalMiddle AgedNerve RegenerationNeurogliaNeuronsReceptors, G-Protein-CoupledYoung AdultGPR17 protein, humanReceptors, G-Protein-Coupled

Identifiers

PMID23801362
PMCPMC3757149
OpenAlexW2019934757

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.