Evidence map›Paper›PMID 24836816›Full record

ArticlePloS one2014

Differential regulation of glutamate transporter subtypes by pro-inflammatory cytokine TNF-α in cortical astrocytes from a rat model of amyotrophic lateral sclerosis.

Amélie O Dumont, Stéphanie Goursaud, Nathalie Desmet, Emmanuel Hermans

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02325375 (Inflammation in Amyotrophic Lateral Sclerosis - a Study of Soluble Cluster of Differentiation 163 in the Cerebrospinal Fluid), which is not on this map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 21% 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.

NCT02325375 completednot on this map

Inflammation in Amyotrophic Lateral Sclerosis - a Study of Soluble Cluster of Differentiation 163 in the Cerebrospinal Fluid

TypeobservationalSponsorUniversity of AarhusRan2014 to 2016Enrolled20ConditionsAmyotrophic Lateral SclerosisArmslumbar puncture for spinal fluid and blood sample
3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 34 citations in OpenAlex.

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  10. Role of Aβ in Alzheimer's-related synaptic dysfunction.Frontiers in cell and developmental biology · 2022
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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

4 authors at 1 institution in 1 country.

Amélie O DumontInstitute of Neuroscience, Group of Neuropharmacology, Université Catholique de Louvain, Brussels, Belgium.
Stéphanie GoursaudInstitute of Neuroscience, Group of Neuropharmacology, Université Catholique de Louvain, Brussels, Belgium.
Nathalie DesmetInstitute of Neuroscience, Group of Neuropharmacology, Université Catholique de Louvain, Brussels, Belgium.
Emmanuel HermansInstitute of Neuroscience, Group of Neuropharmacology, Université Catholique de Louvain, Brussels, Belgium.
UCLouvain · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulation of the astroglial glutamate transporters GLAST and GLT-1 has been implicated in several neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS) where a loss of GLT-1 protein expression and activity is reported. Furthermore, the two principal C-terminal splice variants of GLT-1 (namely GLT-1a and GLT-1b) show altered expression ratio in animal models of this disease. Considering the putative link between inflammation and excitotoxicity, we have here characterized the influence of TNF-α on glutamate transporters in cerebral cortical astrocyte cultures from wild-type rats and from a rat model of ALS (hSOD1G93A). Contrasting with the down-regulation of GLAST, a 72 h treatment with TNF-α substantially increased the expression of GLT-1a and GLT-1b in both astrocyte cultures. However, as the basal level of GLT-1a appeared considerably lower in hSOD1G93A astrocytes, its up-regulation by TNF-α was insufficient to recapitulate the expression observed in wild-type astrocytes. Also the glutamate uptake activity after TNF-α treatment was lower for hSOD1G93A astrocytes as compared to wild-type astrocytes. In the presence of the protein synthesis inhibitor cycloheximide, TNF-α did not influence GLT-1 isoform expression, suggesting an active role of dynamically regulated protein partners in the adaptation of astrocytes to the inflammatory environment. Confirming the influence of inflammation on the control of glutamate transmission by astrocytes, these results shed light on the regulation of glutamate transporter isoforms in neurodegenerative disorders.

Indexed as

Gene Expression RegulationAmino Acid Transport System X-AGAmyotrophic Lateral SclerosisAnimalsAstrocytesCells, CulturedCerebellar CortexCycloheximideCytokinesDisease Models, AnimalInflammationMaleProtein BiosynthesisProtein IsoformsRats, Sprague-DawleyRecombinant ProteinsAmino Acid Transport System X-AGCycloheximideCytokinesProtein IsoformsRecombinant ProteinsSod1 protein, ratSuperoxide DismutaseSuperoxide Dismutase-1Tumor Necrosis Factor-alpha

Identifiers

PMID24836816
PMCPMC4023965
OpenAlexW2018101299

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Registered trials

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.