Hostname: page-component-586b7cd67f-dlnhk Total loading time: 0 Render date: 2024-11-24T11:32:34.230Z Has data issue: false hasContentIssue false

The Role of Micrornas in Regulating Redox Modulation in Bipolar Disorder

Published online by Cambridge University Press:  23 March 2020

H. Kim
Affiliation:
Queen's University, Pathology and Molecular medicine, Kingston, Canada
K. Tyryshkin
Affiliation:
Queen's University, Pathology and Molecular medicine, Kingston, Canada
N. Elmi
Affiliation:
Queen's University, Pathology and Molecular medicine, Kingston, Canada
V. Oliviera
Affiliation:
University of Toronto, Department of Psychiatry, Toronto, Canada
A. Andreazza
Affiliation:
University of Toronto, Departments of Pharmacology and Psychiatry, Toronto, Canada
H. Feilotter
Affiliation:
Queen's University, Pathology and Molecular medicine, Kingston, Canada

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Introduction

Alterations in redox modulation are consistently reported in bipolar disorder (BD). MicroRNAs are targeted regulators of gene expression.

Objectives and aims

We aimed to examine if microRNAs that target redox modulators can discriminate between BD and healthy controls.

Methods

Data from brains of individuals with and without BD were obtained from Array Collection datasets. MicroRNAs targeting redox modulators were assessed for their ability to discriminate BD from the control group using machine-learning algorithms. Methylation of microRNAs, expression of their transcription factors and redox targets were assessed with ANCOVA with FDR correction. For validation, we acquired plasma samples belonging to 2 families of individuals with and without BD (n = 9). Plasma microRNAs were sequenced using the Ion Total RNA Sequencing Kit (Thermo Fisher Scientific), and microRNAs identified from the in silico analysis were examined in the validation dataset.

Results

We identified 5 miRNAs (hsa-miR-299, hsa-miR-125a, hsa-miR-145, hsa-miR-30b, hsa-miR424) that were common in two of the four in silico datasets. Target genes glutathione peroxidase 4, ATP5A1, ATP5G1, NDUFS1, NDUFC2, and catalase were expressed at different levels between BD and the control group. Furthermore, our results showed that transcription factors CTCF and USF1 might control the expression of hsa-miR-145, while methylation differences were not found. Finally, hsa-miR-30b was significantly increased in the plasma of patients with BD compared to controls in the validation experiment.

Conclusions

Our study demonstrates that microRNAs may have an important role in the initiation of redox changes in BD.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
e-Poster walk: Anxiety disorders and somatoform disorders
Copyright
Copyright © European Psychiatric Association 2017
Submit a response

Comments

No Comments have been published for this article.