Evidence map›Paper›PMID 23804112›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Estrogen mediates neuroprotection and anti-inflammatory effects during EAE through ERα signaling on astrocytes but not through ERβ signaling on astrocytes or neurons.

Rory D Spence, Amy J Wisdom, Yuan Cao, Haley M Hill, Chandler R L Mongerson, Briana Stapornkul, Noriko Itoh, Michael V Sofroniew, Rhonda R Voskuhl

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 175 citations in OpenAlex.

  1. Article
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  9. Astrocyte involvement in metabolic regulation and disease.Trends in endocrinology and metabolism: TEM · 2025
    Review
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  15. Article
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  18. The Influence of Sex Hormones and X Chromosome in Immune Responses.Current topics in microbiology and immunology · 2023
    Review
  19. Review
  20. Review

34 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

9 authors at 1 institution in 1 country.

Rory D SpenceDepartments of Neurology and Neurobiology, University of California Los Angeles, Multiple Sclerosis Program, Los Angeles, California 90095, USA.
Amy J Wisdom
Yuan Cao
Haley M Hill
Chandler R L Mongerson
Briana Stapornkul
Noriko Itoh
Michael V Sofroniew
Rhonda R Voskuhl
University of California, Los Angeles · US

Funding

Neuroendocrinology, Sex Differences, and ReproductionT32HD007228 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 1985 to 2015
$3.9M
Training in Molecular, Cellular &Integrative PhysiologyT32GM065823 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2003 to 2017
$2.1M
Treatment of Multiple Sclerosis with Sex HormonesK24NS062117 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI VOSKUHL, RHONDA R · 2008 to 2012
$722k
CSR NIH HHS RG 4364Howard Hughes Medical InstituteNICHD NIH HHS T32 HD007228NICHD NIH HHS T32 HD 7228-31NIGMS NIH HHS T32 GM065823NINDS NIH HHS K24 NS062117NINDS NIH HHS R01 K24 NS 062117
6 · The paper itself

Abstract

Estrogens can signal through either estrogen receptor α (ERα) or β (ERβ) to ameliorate experimental autoimmune encephalomyelitis (EAE), the most widely used mouse model of multiple sclerosis (MS). Cellular targets of estrogen-mediated neuroprotection are still being elucidated. Previously, we demonstrated that ERα on astrocytes, but not neurons, was critical for ERα ligand-mediated neuroprotection in EAE, including decreased T-cell and macrophage inflammation and decreased axonal loss. Here, we determined whether ERβ on astrocytes or neurons could mediate neuroprotection in EAE, by selectively removing ERβ from either of these cell types using Cre-loxP gene deletion. Our results demonstrated that, even though ERβ ligand treatment was neuroprotective in EAE, this neuroprotection was not mediated through ERβ on either astrocytes or neurons and did not involve a reduction in levels of CNS inflammation. Given the differential neuroprotective and anti-inflammatory effects mediated via ERα versus ERβ on astrocytes, we looked for molecules within astrocytes that were affected by signaling through ERα, but not ERβ. We found that ERα ligand treatment, but not ERβ ligand treatment, decreased expression of the chemokines CCL2 and CCL7 by astrocytes in EAE. Together, our data show that neuroprotection in EAE mediated via ERβ signaling does not require ERβ on either astrocytes or neurons, whereas neuroprotection in EAE mediated via ERα signaling requires ERα on astrocytes and reduces astrocyte expression of proinflammatory chemokines. These findings reveal important cellular differences in the neuroprotective mechanisms of estrogen signaling through ERα and ERβ in EAE.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalNeuroprotective AgentsAnimalsAquaporin 4AstrocytesAxonsCell CountChemokine CCL2Chemokine CCL7Demyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalEstrogen Receptor alphaEstrogen Receptor betaEstrogensGliosisImmunohistochemistryAnti-Inflammatory Agents, Non-SteroidalAquaporin 4Chemokine CCL2Chemokine CCL7Estrogen Receptor alphaEstrogen Receptor betaEstrogensNeuroprotective Agents

Identifiers

PMID23804112
PMCPMC3693061
OpenAlexW1726588509

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.