Evidence map›Paper›PMID 19890015›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010

Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration.

Eva K Wirth, Marcus Conrad, Jochen Winterer, Christian Wozny, Bradley A Carlson, Stephan Roth, Dietmar Schmitz, Georg W Bornkamm, Vincenzo Coppola, Lino Tessarollo and 4 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

107 citing papers in PubMed, 236 citations in OpenAlex.

  1. Review
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  3. Review
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  5. Fueling Death: The Metabolic Control of Ferroptosis.Advances in experimental medicine and biology · 2026
    Review
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  7. Recommendations for robust and reproducible research on ferroptosis.Nature reviews. Molecular cell biology · 2025
    Review
  8. Article
  9. Neuroferroptosis in health and diseases.Nature reviews. Neuroscience · 2025
    Review
  10. Article
  11. Review
  12. Ferroptosis and Pyroptosis in Epilepsy.Molecular neurobiology · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Deciphering the Role of Selenoprotein M.Antioxidants (Basel, Switzerland) · 2023
    Review
  18. "Alphabet" Selenoproteins: Implications in Pathology.International journal of molecular sciences · 2023
    Review
  19. Review
  20. Article

47 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

14 authors at 7 institutions in 4 countries.

Eva K WirthInstitute for Experimental Endocrinology, Charité-Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.
Marcus Conrad
Jochen Winterer
Christian Wozny
Bradley A Carlson
Stephan Roth
Dietmar Schmitz
Georg W Bornkamm
Vincenzo Coppola
Lino Tessarollo
Lutz Schomburg
Josef Köhrle
Dolph L Hatfield
Ulrich Schweizer
Charité - Universitätsmedizin Berlin · DEHelmholtz Zentrum München · DEBioscience Research · USCancer Institute (WIA) · INCenter for Cancer Research · USNational Cancer Institute · USNational Institutes of Health · US

Funding

Role of Selenium in Development and HealthZIABC005317 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HATFIELD, DOLPH · 2009 to 2014
$2.7M
Intramural NIH HHS
6 · The paper itself

Abstract

Cerebral selenium (Se) deficiency is associated with neurological phenotypes including seizures and ataxia. We wanted to define whether neurons require selenoprotein expression and which selenoproteins are most important, and explore the possible pathomechanism. Therefore, we abrogated the expression of all selenoproteins in neurons by genetic inactivation of the tRNA[Ser](Sec) gene. Cerebral expression of selenoproteins was significantly diminished in the mutants, and histological analysis revealed progressive neurodegeneration. Developing interneurons failed to specifically express parvalbumin (PV) in the mutants. Electrophysiological recordings, before overt cell death, showed normal excitatory transmission, but revealed spontaneous epileptiform activity consistent with seizures in the mutants. In developing cortical neuron cultures, the number of PV(+) neurons was reduced on combined Se and vitamin E deprivation, while other markers, such as calretinin (CR) and GAD67, remained unaffected. Because of the synergism between Se and vitamin E, we analyzed mice lacking neuronal expression of the Se-dependent enzyme glutathione peroxidase 4 (GPx4). Although the number of CR(+) interneurons remained normal in Gpx4-mutant mice, the number of PV(+) interneurons was reduced. Since these mice similarly exhibit seizures and ataxia, we conclude that GPx4 is a selenoenzyme modulating interneuron function and PV expression. Cerebral SE deficiency may thus act via reduced GPx4 expression.-Wirth, E. K., Conrad, M., Winterer, J., Wozny, C., Carlson, B. A., Roth, S., Schmitz, D., Bornkamm, G. W., Coppola, V., Tessarollo, L., Schomburg, L., Köhrle, J., Hatfield, D. L., Schweizer, U. Neuronal selenoprotein expression is required for interneuron development and prevents seizures and neurodegeneration.

Indexed as

AnimalsBlotting, WesternCalbindin 2Cell DifferentiationCells, CulturedElectrophysiologyGlutathione PeroxidaseImmunohistochemistryInterneuronsMiceMice, KnockoutNerve DegenerationParvalbuminsPhospholipid Hydroperoxide Glutathione PeroxidaseRNA, Transfer, Amino AcylS100 Calcium Binding Protein GCalb2 protein, mouseCalbindin 2Glutathione PeroxidaseParvalbuminsPhospholipid Hydroperoxide Glutathione PeroxidaseRNA, Transfer, Amino AcylS100 Calcium Binding Protein GSeleniumselenocysteinyl-tRNASelenoproteinsVitamin E

Identifiers

PMID19890015
PMCPMC2830140
OpenAlexW2143099403

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.