Evidence map›Paper›PMID 23959066›Full record

ArticleEpigenetics2014

Prenatal stress changes the glycoprotein GPM6A gene expression and induces epigenetic changes in rat offspring brain.

Melisa C Monteleone, Ezequiela Adrover, María Eugenia Pallarés, Marta C Antonelli, Alberto C Frasch, Marcela A Brocco

Abstract read
In one paragraph

Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

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  15. Article
  16. The epigenetics of perinatal stress
.Dialogues in clinical neuroscience · 2019
    Review
  17. Review
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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

6 authors.

Melisa C MonteleoneInstituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomus (IIB-INTECH); Universidad Nacional de San Martín (UNSAM); Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) San Martín; Buenos Aires, Argentina.
Ezequiela AdroverIQUIFIB; Facultad de Farmacia y Bioquímica; Universidad de Buenos Aires; Buenos Aires, Argentina.
María Eugenia PallarésIQUIFIB; Facultad de Farmacia y Bioquímica; Universidad de Buenos Aires; Buenos Aires, Argentina.
Marta C AntonelliIQUIFIB; Facultad de Farmacia y Bioquímica; Universidad de Buenos Aires; Buenos Aires, Argentina.
Alberto C FraschInstituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomus (IIB-INTECH); Universidad Nacional de San Martín (UNSAM); Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) San Martín; Buenos Aires, Argentina.
Marcela A BroccoInstituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomus (IIB-INTECH); Universidad Nacional de San Martín (UNSAM); Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) San Martín; Buenos Aires, Argentina.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal stress (PS) exerts strong impact on fetal brain development and on adult offspring brain functions. Previous work demonstrated that chronic stress alters the mRNA expression of GPM6A, a neuronal glycoprotein involved in filopodium extension. In this work, we analyzed the effect of PS on gpm6a expression and the epigenetic mechanisms involved. Pregnant Wistar rats received restraint stress during the last week of gestation. Male offspring were sacrificed on postnatal days 28 and 60. Hippocampus and prefrontal cortex samples were analyzed for gene expression (qPCR for mRNAs and microRNAs), methylation status (bisulfite conversion) and protein levels. Hippocampal neurons in culture were used to analyze microRNA overexpression effects. Prenatal stress induced changes in gpm6a levels in both tissues and at both ages analyzed, indicating a persistent effect. Two CpG islands in the gpm6a gene were identified. Variations in the methylation pattern at three specific CpGs were found in hippocampus, but not in PFC samples from PS offspring. microRNAs predicted to target gpm6a were identified in silico. qPCR measurements showed that PS modified the expression of several microRNAs in both tissues, being microRNA-133b the most significantly altered. Further studies overexpressing this microRNA in neuronal cultures showed a reduction in gmp6a mRNA and protein level. Moreover filopodium density was also reduced, suggesting that GPM6A function was affected. Gestational stress affected gpm6a gene expression in offspring likely through changes in methylation status and in posttranscriptional regulation by microRNAs. Thus, our findings propose gpm6a as a novel target for epigenetic regulation during prenatal stress.

Indexed as

Epigenesis, GeneticAnimalsBrainCells, CulturedCpG IslandsFemaleGlycoproteinsHippocampusMaleMembrane GlycoproteinsMethylationMicroRNAsNerve Tissue ProteinsNeuronsPrefrontal CortexPregnancyGlycoproteinsGpm6a protein, ratMembrane GlycoproteinsMicroRNAsMIRN133 microRNA, ratNerve Tissue ProteinsCpG islandDNA methylation patternhippocampusmicroRNAprefrontal cortextarget site blocker

Identifiers

PMID23959066
PMCPMC3928178

What OpenQuestion holds

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Registered trials

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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.