Evidence map›Paper›PMID 25927603›Full record

ArticlePloS one2015

The Receptor CMRF35-Like Molecule-1 (CLM-1) Enhances the Production of LPS-Induced Pro-Inflammatory Mediators during Microglial Activation.

Aroa Ejarque-Ortiz, Carme Solà, Águeda Martínez-Barriocanal, Simó Schwartz, Margarita Martín, Hugo Peluffo, Joan Sayós

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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  6. CD300f immunoreceptor is associated with major depressive disorder and decreased microglial metabolic fitness.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 6 institutions in 2 countries.

Aroa Ejarque-OrtizImmunobiology Group, CIBBIM-Nanomedicine Program, Hospital Universitari Vall d'Hebrón, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBBER-BBN), Instituto de Salud Carlos III, Barcelona, Spain.
Carme SolàDepartment of Cerebral Ischemia and Neurodegeneration, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas (CSIC), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Águeda Martínez-BarriocanalImmunobiology Group, CIBBIM-Nanomedicine Program, Hospital Universitari Vall d'Hebrón, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBBER-BBN), Instituto de Salud Carlos III, Barcelona, Spain.
Simó SchwartzDrug Delivery and Targeting Group, CIBBIM-Nanomedicine Program, Hospital Universitari Vall d'Hebrón, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBBER-BBN), Instituto de Salud Carlos III, Barcelona, Spain.
Margarita MartínBiochemistry Unit, Faculty of Medicine, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Hugo PeluffoNeurodegeneration Laboratory, Institut Pasteur de Montevideo, Montevideo, Uruguay; Department of Histology and Embryology, Faculty of Medicine, UDELAR, Montevideo, Uruguay.
Joan SayósImmunobiology Group, CIBBIM-Nanomedicine Program, Hospital Universitari Vall d'Hebrón, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, Barcelona, Spain; Networking Research Center on Bioengineering, Biomaterials and Nanomedicine (CIBBER-BBN), Instituto de Salud Carlos III, Barcelona, Spain.
Vall d'Hebron Institut de Recerca · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Salud Carlos III · ESInstitut Pasteur de Montevideo · UYUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CMRF35-like molecule-1 (CLM-1) belongs to a receptor family mainly expressed in myeloid cells that include activating and inhibitory receptors. CLM-1 contains two ITIMs and a single immunoreceptor tyrosine-based switch motif (ITSM), although also displays a binding site for p85α regulatory subunit of PI3K. By using murine primary microglial cultures, we show the presence of all CLM members in microglial cells and characterize the expression of CLM-1 both in basal conditions and during microglial activation. The TLR4 agonist lipopolysaccharide (LPS) and the TLR3 agonist polyinosinic-polycytidylic acid (Poly I:C) induce an increase in microglial CLM-1 mRNA levels in vitro, whereas the TLR2/6 heterodimer agonist peptidoglycan (PGN) produces a marked decrease. In this study we also describe a new soluble isoform of CLM-1 that is detected at mRNA and protein levels in basal conditions in primary microglial cultures. Interestingly, CLM-1 engagement enhances the transcription of the pro-inflammatory mediators TNFα, COX-2 and NOS-2 in microglial cells challenged with LPS. These results reveal that CLM-1 can acts as a co-activating receptor and suggest that this receptor could play a key role in the regulation of microglial activation.

Indexed as

AnimalsChlorocebus aethiopsCOS CellsCyclooxygenase 2Gene Expression RegulationInflammation MediatorsLipopolysaccharidesMiceMicrogliaNIH 3T3 CellsNitric Oxide Synthase Type IIPhosphatidylinositol 3-KinasesPoly I-CReceptors, ImmunologicToll-Like ReceptorsTumor Necrosis Factor-alphaCLM-1 protein, mouseCyclooxygenase 2Inflammation MediatorsLipopolysaccharidesNitric Oxide Synthase Type IINos2 protein, mousePhosphatidylinositol 3-KinasesPoly I-CPtgs2 protein, mouseReceptors, ImmunologicToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID25927603
PMCPMC4415817
OpenAlexW2060530138

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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.