ArticleExperimental and therapeutic medicine2014
Tumor necrosis factor-α promotes the expression of excitatory amino-acid transporter 2 in astrocytes: Optimal concentration and incubation time.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes.Cytotechnology · 2025Review
- Soybean glycinin decreased growth performance, impaired intestinal health, and amino acid absorption capacity of juvenile grass carp (Ctenopharyngodon idella).Fish physiology and biochemistry · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to determine whether tumor necrosis factor (TNF)-α regulates the expression levels of excitatory amino-acid transporters (EAATs) in primary astrocytes and its roles in brain ischemia. Exogenous TNF-α was administered to pure cultured astrocytes and the expression levels of EAAT1, EAAT2 and glial fibrillary acidic protein (GFAP) were evaluated. The results showed that TNF-α at 10 ng/ml enhanced the expression of EAAT2 in a time-dependent manner, while the expression levels of EAAT1 and GFAP did not change. To determine whether the elevation in the levels of the EAAT2 protein induced by TNF-α had a beneficial effect on ischemic insult, TNF-α was applied to
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