Evidence map›Paper›PMID 29686286›Full record

ArticleNature communications2018

Placental miR-340 mediates vulnerability to activity based anorexia in mice.

Mariana Schroeder, Mira Jakovcevski, Tamar Polacheck, Yonat Drori, Alessia Luoni, Simone Röh, Jonas Zaugg, Shifra Ben-Dor, Christiane Albrecht, Alon Chen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
11.3field-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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Animal Models for Anorexia Nervosa-A Systematic Review.Frontiers in human neuroscience · 2020
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  10. Regulation of PVT-CeA Circuit in Deoxynivalenol-Induced Anorexia and Aversive-Like Emotions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

10 authors at 3 institutions in 3 countries.

Mariana SchroederDepartment of Neurobiology, Weizmann Institute of Science, 7610001, Rehovot, Israel. mariana_schroeder@psych.mpg.de.
Mira JakovcevskiDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, 80804, Munich, Germany.ORCID http://orcid.org/0000-0003-2262-823X
Tamar PolacheckDepartment of Neurobiology, Weizmann Institute of Science, 7610001, Rehovot, Israel.
Yonat DroriDepartment of Neurobiology, Weizmann Institute of Science, 7610001, Rehovot, Israel.
Alessia LuoniDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, 80804, Munich, Germany.
Simone RöhDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, 80804, Munich, Germany.
Jonas ZauggInstitute of Biochemistry and Molecular Medicine, University of Bern, 3012, Bern, Switzerland.
Shifra Ben-DorBioinformatics and Biological Computing Unit, Biological Services, Weizmann Institute of Science, 7610001, Rehovot, Israel.ORCID http://orcid.org/0000-0001-9604-1939
Christiane AlbrechtInstitute of Biochemistry and Molecular Medicine, University of Bern, 3012, Bern, Switzerland.ORCID http://orcid.org/0000-0002-7846-6930
Alon ChenDepartment of Neurobiology, Weizmann Institute of Science, 7610001, Rehovot, Israel. alon_chen@psych.mpg.de.ORCID http://orcid.org/0000-0003-3625-8233
Max Planck Institute of Psychiatry · DEUniversity of Bern · CHWeizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anorexia nervosa (AN) is a devastating eating disorder characterized by self-starvation that mainly affects women. Its etiology is unknown, which impedes successful treatment options leading to a limited chance of full recovery. Here, we show that gestation is a vulnerable window that can influence the predisposition to AN. By screening placental microRNA expression of naive and prenatally stressed (PNS) fetuses and assessing vulnerability to activity-based anorexia (ABA), we identify miR-340 as a sexually dimorphic regulator involved in prenatal programming of ABA. PNS caused gene-body hypermethylation of placental miR-340, which is associated with reduced miR-340 expression and increased protein levels of several target transcripts, GR, Cry2 and H3F3b. MiR-340 is linked to the expression of several nutrient transporters both in mice and human placentas. Using placenta-specific lentiviral transgenes and embryo transfer, we demonstrate the key role miR-340 plays in the mechanism involved in early life programming of ABA.

Indexed as

AdultAnimalsAnorexia NervosaCell Line, TumorDisease Models, AnimalEmbryo TransferFemaleGene Expression Regulation, DevelopmentalGenetic Predisposition to DiseaseHumansMaleMaternal-Fetal ExchangeMiceMice, Inbred ICRMice, TransgenicMicroRNAsMicroRNAsMIRN340 microRNA, humanMIRN340 microRNA, mouse

Identifiers

PMID29686286
PMCPMC5913294
OpenAlexW2803039419

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.