Evidence map›Paper›PMID 20200508›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2010

Adenosine A1 receptors and microglial cells mediate CX3CL1-induced protection of hippocampal neurons against Glu-induced death.

Clotilde Lauro, Raffaela Cipriani, Myriam Catalano, Flavia Trettel, Giuseppina Chece, Valentina Brusadin, Letizia Antonilli, Nico van Rooijen, Fabrizio Eusebi, Bertil B Fredholm and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Upregulation of Chemokines in the Paraventricular Nucleus of the Hypothalamus in Rats with Stress-Induced Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  17. Review
  18. Article
  19. Cordycepin protects against β-amyloid and ibotenic acid-induced hippocampal CA1 pyramidal neuronal hyperactivity.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019
    Article
  20. Protective effects of CX3CR1 on autoimmune inflammation in a chronic EAE model for MS through modulation of antigen-presenting cell-related molecular MHC-II and its regulators.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article

2 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 3 countries.

Clotilde LauroIstituto Pasteur, Fondazione Cenci Bolognetti, Rome, Italy.
Raffaela Cipriani
Myriam Catalano
Flavia Trettel
Giuseppina Chece
Valentina Brusadin
Letizia Antonilli
Nico van Rooijen
Fabrizio Eusebi
Bertil B Fredholm
Cristina Limatola
Sapienza University of Rome · ITIstituto Pasteur · ITAcademic Medical Center · NLKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fractalkine/CX3CL1 is a neuron-associated chemokine, which modulates microglia-induced neurotoxicity activating the specific and unique receptor CX3CR1. CX3CL1/CX3CR1 interaction modulates the release of cytokines from microglia, reducing the level of tumor necrosis factor-alpha, interleukin-1-beta, and nitric oxide and induces the production of neurotrophic substances, both in vivo and in vitro. We have recently shown that blocking adenosine A(1) receptors (A(1)R) with the specific antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) abolishes CX3CL1-mediated rescue of neuronal excitotoxic death and that CX3CL1 induces the release of adenosine from microglia. In this study, we show that the presence of extracellular adenosine is mandatory for the neurotrophic effect of CX3CL1 as reducing adenosine levels in hippocampal cultures, by adenosine deaminase treatment, strongly impairs CX3CL1-mediated neuroprotection. Furthermore, we confirm the predominant role of microglia in mediating the neuronal effects of CX3CL1, because the selective depletion of microglia from hippocampal cultures treated with clodronate-filled liposomes causes the complete loss of effect of CX3CL1. We also show that hippocampal neurons obtained from A(1)R(-/-) mice are not protected by CX3CL1 whereas A(2A)R(-/-) neurons are. The requirement of functional A(1)R for neuroprotection is not unique for CX3CL1 as A(1)R(-/-) hippocampal neurons are not rescued from Glu-induced cell death by other neurotrophins such as brain-derived neurotrophic factor and erythropoietin, which are fully active on wt neurons.

Indexed as

AdenosineAdenosine A1 Receptor AntagonistsAdenosine DeaminaseAdenosine DiphosphateAnimalsAnimals, NewbornBrain-Derived Neurotrophic FactorCell DeathCell MovementClodronic AcidCX3C Chemokine Receptor 1ErythropoietinGlutamic AcidGreen Fluorescent ProteinsHippocampusMice1,3-dipropyl-8-cyclopentylxanthineAdenosineAdenosine A1 Receptor AntagonistsAdenosine DeaminaseAdenosine Diphosphatealpha,beta-methyleneadenosine 5'-diphosphateBrain-Derived Neurotrophic FactorClodronic AcidCX3C Chemokine Receptor 1Cx3cr1 protein, mouseErythropoietinGlutamic AcidGreen Fluorescent ProteinsReceptor, Adenosine A1Receptors, Adenosine A2Receptors, ChemokineXanthines

Identifiers

PMID20200508
PMCPMC3055460
OpenAlexW2106903618

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.