Evidence map›Paper›PMID 25268256›Full record

ArticleTranslational psychiatry2014

Alteration of imprinted Dlk1-Dio3 miRNA cluster expression in the entorhinal cortex induced by maternal immune activation and adolescent cannabinoid exposure.

S L Hollins, K Zavitsanou, F R Walker, M J Cairns

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

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  17. Transgenerational modification of dopaminergic dysfunctions induced by maternal immune activation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
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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

4 authors at 3 institutions in 1 country.

S L Hollins1] School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia [2] Schizophrenia Research Institute, Sydney, NSW, Australia [3] Hunter Medical Research Institute, Newcastle, NSW, Australia.
K Zavitsanou1] School of Psychiatry, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia [2] Schizophrenia Research Laboratory, Neuroscience Research Australia, Randwick, NSW, Australia.
F R Walker1] School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia [2] The Centre for Translational Neuroscience and Mental Health, Callaghan, NSW, Australia.
M J Cairns1] School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia [2] Schizophrenia Research Institute, Sydney, NSW, Australia [3] Hunter Medical Research Institute, Newcastle, NSW, Australia.
University of Newcastle Australia · AUSchizophrenia Research Institute · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significant feature of the cortical neuropathology of schizophrenia is a disturbance in the biogenesis of short non-coding microRNA (miRNA) that regulate translation and stability of mRNA. While the biological origin of this phenomenon has not been defined, it is plausible that it relates to major environmental risk factors associated with the disorder such as exposure to maternal immune activation (MIA) and adolescent cannabis use. To explore this hypothesis, we administered the viral mimic poly I:C to pregnant rats and further exposed some of their maturing offsprings to daily injections of the synthetic cannabinoid HU210 for 14 days starting on postnatal day 35. Whole-genome miRNA expression analysis was then performed on the left and right hemispheres of the entorhinal cortex (EC), a region strongly associated with schizophrenia. Animals exposed to either treatment alone or in combination exhibited significant differences in the expression of miRNA in the left hemisphere, whereas the right hemisphere was less responsive. Hemisphere-associated differences in miRNA expression were greatest in the combined treatment and highly over-represented in a single imprinted locus on chromosome 6q32. This observation was significant as the syntenic 14q32 locus in humans encodes a large proportion of miRNAs differentially expressed in peripheral blood lymphocytes from patients with schizophrenia, suggesting that interaction of early and late environmental insults may affect miRNA expression, in a manner that is relevant to schizophrenia.

Indexed as

Entorhinal CortexAnimalsCannabinoidsFemaleGene ExpressionGenomic ImprintingHumansInfant, NewbornIntercellular Signaling Peptides and ProteinsIodide PeroxidaseMaleMaternal ExposureMembrane ProteinsMicroRNAsPregnancyPrenatal Exposure Delayed EffectsCannabinoidsDlk1 protein, ratIntercellular Signaling Peptides and ProteinsIodide Peroxidaseiodothyronine deiodinase type IIIMembrane ProteinsMicroRNAs

Identifiers

PMID25268256
PMCPMC4203021
OpenAlexW1964248550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.