Evidence map›Paper›PMID 38792584›Full record

ArticleLife (Basel, Switzerland)2024

microRNA and the Post-Transcriptional Response to Oxidative Stress during Neuronal Differentiation: Implications for Neurodevelopmental and Psychiatric Disorders.

Behnaz Khavari, Michelle M Barnett, Ebrahim Mahmoudi, Michael P Geaghan, Adam Graham, Murray J Cairns

Abstract read
In one paragraph

Article in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Behnaz KhavariSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.
Michelle M BarnettSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.ORCID 0000-0002-2621-8302
Ebrahim MahmoudiSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.ORCID 0000-0001-6506-0491
Michael P GeaghanSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.
Adam GrahamSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.
Murray J CairnsSchool of Biomedical Sciences and Pharmacy, The University of Newcastle, Callaghan, NSW 2308, Australia.ORCID 0000-0003-2490-2538

Funding

National Health and Medical Research Council 1067137National Health and Medical Research Council 1121474
6 · The paper itself

Abstract

Oxidative stress is one of the most important environmental exposures associated with psychiatric disorders, but the underlying molecular mechanisms remain to be elucidated. In a previous study, we observed a substantial alteration of the gene expression landscape in neuron-like cells that were differentiated from SH-SY5Y cells after or during exposure to oxidative stress, with a subset of dysregulated genes being enriched for neurodevelopmental processes. To further explore the regulatory mechanisms that might account for such profound perturbations, we have now applied small RNA-sequencing to investigate changes in the expression of miRNAs. These molecules are known to play crucial roles in brain development and response to stress through their capacity to suppress gene expression and influence complex biological networks. Through these analyses, we observed more than a hundred differentially expressed miRNAs, including 80 previously reported to be dysregulated in psychiatric disorders. The seven most influential miRNAs associated with pre-treatment exposure, including miR-138-5p, miR-96-5p, miR-34c-5p, miR-1287-5p, miR-497-5p, miR-195-5p, and miR-16-5p, supported by at least 10 negatively correlated mRNA connections, formed hubs in the interaction network with 134 genes enriched with neurobiological function, whereas in the co-treatment condition, miRNA-mRNA interaction pairs were enriched in cardiovascular and immunity-related disease ontologies. Interestingly, 12 differentially expressed miRNAs originated from the DLK1-DIO3 location, which encodes a schizophrenia-associated miRNA signature. Collectively, our findings suggest that early exposure to oxidative stress, before and during prenatal neuronal differentiation, might increase the risk of mental illnesses in adulthood by disturbing the expression of miRNAs that regulate neurodevelopmentally significant genes and networks.

Indexed as

DLK1-DIO3immune systemmiR-137miR-181bmiRNAneurodevelopmentoxidative stresspsychiatric disorders

Identifiers

PMID38792584
PMCPMC11121913

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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.