Evidence map›Paper›PMID 28894299›Full record

ArticleMolecular psychiatry2018

DHEA inhibits acute microglia-mediated inflammation through activation of the TrkA-Akt1/2-CREB-Jmjd3 pathway.

V I Alexaki, G Fodelianaki, A Neuwirth, C Mund, A Kourgiantaki, E Ieronimaki, K Lyroni, M Troullinaki, C Fujii, W Kanczkowski and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 99 citations in OpenAlex.

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  9. Effects ofJournal of microbiology and biotechnology · 2025
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  13. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
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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

19 authors at 4 institutions in 3 countries.

V I AlexakiInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
G FodelianakiInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
A NeuwirthInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
C MundInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
A KourgiantakiDepartment of Pharmacology, Medical School, University of Crete, Heraklion, Greece.
E IeronimakiDepartment of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.
K LyroniDepartment of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.
M TroullinakiInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
C FujiiInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
W KanczkowskiInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
A ZiogasInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
M PeitzschInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
S GrossklausInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
B SönnichsenLife Science Inkubator Sachsen GmbH & Co. KG, Dresden, Germany.
A GravanisDepartment of Pharmacology, Medical School, University of Crete, Heraklion, Greece.
S R BornsteinDepartment of Internal Medicine III, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
I CharalampopoulosDepartment of Pharmacology, Medical School, University of Crete, Heraklion, Greece.
C TsatsanisDepartment of Clinical Chemistry, Medical School, University of Crete, Heraklion, Greece.
T ChavakisInstitute for Clinical Chemistry and Laboratory Medicine, University Clinic Carl Gustav Carus, TU Dresden, Dresden, Germany.
TU Dresden · DEUniversity Hospital Carl Gustav Carus · DEUniversity of Crete · GRFoundation for Research and Technology Hellas · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dehydroepiandrosterone (DHEA) is the most abundant circulating steroid hormone in humans, produced by the adrenals, the gonads and the brain. DHEA was previously shown to bind to the nerve growth factor receptor, tropomyosin-related kinase A (TrkA), and to thereby exert neuroprotective effects. Here we show that DHEA reduces microglia-mediated inflammation in an acute lipopolysaccharide-induced neuro-inflammation model in mice and in cultured microglia in vitro. DHEA regulates microglial inflammatory responses through phosphorylation of TrkA and subsequent activation of a pathway involving Akt1/Akt2 and cAMP response element-binding protein. The latter induces the expression of the histone 3 lysine 27 (H3K27) demethylase Jumonji d3 (Jmjd3), which thereby controls the expression of inflammation-related genes and microglial polarization. Together, our data indicate that DHEA-activated TrkA signaling is a potent regulator of microglia-mediated inflammation in a Jmjd3-dependent manner, thereby providing the platform for potential future therapeutic interventions in neuro-inflammatory pathologies.

Indexed as

AnimalsCREB-Binding ProteinDehydroepiandrosteroneInflammationJumonji Domain-Containing Histone DemethylasesLipopolysaccharidesMaleMiceMice, Inbred C57BLMicrogliaNeuroprotective AgentsPhosphorylationProto-Oncogene Proteins c-aktReceptors, Nerve Growth FactorReceptor, trkASignal TransductionAkt1 protein, mouseAkt2 protein, mouseCREB-Binding ProteinCrebbp protein, mouseDehydroepiandrosteroneJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouseLipopolysaccharidesNeuroprotective AgentsProto-Oncogene Proteins c-aktReceptors, Nerve Growth FactorReceptor, trkA

Identifiers

PMID28894299
OpenAlexW2756079858

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.