Cargando…

Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis

Multiple sclerosis (MS) is an immune-mediated demyelinating and degenerative disease with unknown etiology. Inappropriate response of T-cells to myelin antigens has an essential role in the pathophysiology of MS. The clinical and pathophysiological complications of MS necessitate identification of p...

Descripción completa

Detalles Bibliográficos
Autores principales: Sabaie, Hani, Salkhordeh, Zoha, Asadi, Mohammad Reza, Ghafouri-Fard, Soudeh, Amirinejad, Nazanin, Askarinejad Behzadi, Mahla, Hussen, Bashdar Mahmud, Taheri, Mohammad, Rezazadeh, Maryam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8696673/
https://www.ncbi.nlm.nih.gov/pubmed/34956196
http://dx.doi.org/10.3389/fimmu.2021.770679
_version_ 1784619869807837184
author Sabaie, Hani
Salkhordeh, Zoha
Asadi, Mohammad Reza
Ghafouri-Fard, Soudeh
Amirinejad, Nazanin
Askarinejad Behzadi, Mahla
Hussen, Bashdar Mahmud
Taheri, Mohammad
Rezazadeh, Maryam
author_facet Sabaie, Hani
Salkhordeh, Zoha
Asadi, Mohammad Reza
Ghafouri-Fard, Soudeh
Amirinejad, Nazanin
Askarinejad Behzadi, Mahla
Hussen, Bashdar Mahmud
Taheri, Mohammad
Rezazadeh, Maryam
author_sort Sabaie, Hani
collection PubMed
description Multiple sclerosis (MS) is an immune-mediated demyelinating and degenerative disease with unknown etiology. Inappropriate response of T-cells to myelin antigens has an essential role in the pathophysiology of MS. The clinical and pathophysiological complications of MS necessitate identification of potential molecular targets to understand the pathogenic events of MS. Since the functions and regulatory mechanisms of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in MS are yet uncertain, we conducted a bioinformatics analysis to explain the lncRNA-associated ceRNA axes to clarify molecular regulatory mechanisms involved in T-cells responses in MS. Two microarray datasets of peripheral blood T-cell from subjects with relapsing-remitting MS and matched controls containing data about miRNAs (GSE43590), mRNAs and lncRNAs (GSE43591) were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs (DEmiRNAs), mRNAs (DEmRNAs), and lncRNAs (DElncRNAs) were identified by the limma package of the R software. Protein-protein interaction (PPI) network and module were developed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) Cytoscape plugin, respectively. Using DIANA-LncBase and miRTarBase, the lncRNA-associated ceRNA axes was constructed. We conducted a Pearson correlation analysis and selected the positive correlations among the lncRNAs and mRNAs in the ceRNA axes. Lastly, DEmRNAs pathway enrichment was conducted by the Enrichr tool. A ceRNA regulatory relationship among Small nucleolar RNA host gene 1 (SNHG1), hsa-miR-197-3p, YOD1 deubiquitinase (YOD1) and zinc finger protein 101 (ZNF101) and downstream connected genes was identified. Pathway enrichment analysis showed that DEmRNAs were enriched in “Protein processing in endoplasmic reticulum” and “Herpes simplex virus 1 infection” pathways. To our knowledge, this would be the first report of a possible role of SNHG1/hsa-miR-197-3p/YOD1/ZNF101 axes in the pathogenesis of MS. This research remarks on the significance of ceRNAs and prepares new perceptions for discovering the molecular mechanism of MS.
format Online
Article
Text
id pubmed-8696673
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-86966732021-12-24 Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis Sabaie, Hani Salkhordeh, Zoha Asadi, Mohammad Reza Ghafouri-Fard, Soudeh Amirinejad, Nazanin Askarinejad Behzadi, Mahla Hussen, Bashdar Mahmud Taheri, Mohammad Rezazadeh, Maryam Front Immunol Immunology Multiple sclerosis (MS) is an immune-mediated demyelinating and degenerative disease with unknown etiology. Inappropriate response of T-cells to myelin antigens has an essential role in the pathophysiology of MS. The clinical and pathophysiological complications of MS necessitate identification of potential molecular targets to understand the pathogenic events of MS. Since the functions and regulatory mechanisms of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in MS are yet uncertain, we conducted a bioinformatics analysis to explain the lncRNA-associated ceRNA axes to clarify molecular regulatory mechanisms involved in T-cells responses in MS. Two microarray datasets of peripheral blood T-cell from subjects with relapsing-remitting MS and matched controls containing data about miRNAs (GSE43590), mRNAs and lncRNAs (GSE43591) were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs (DEmiRNAs), mRNAs (DEmRNAs), and lncRNAs (DElncRNAs) were identified by the limma package of the R software. Protein-protein interaction (PPI) network and module were developed using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and the Molecular Complex Detection (MCODE) Cytoscape plugin, respectively. Using DIANA-LncBase and miRTarBase, the lncRNA-associated ceRNA axes was constructed. We conducted a Pearson correlation analysis and selected the positive correlations among the lncRNAs and mRNAs in the ceRNA axes. Lastly, DEmRNAs pathway enrichment was conducted by the Enrichr tool. A ceRNA regulatory relationship among Small nucleolar RNA host gene 1 (SNHG1), hsa-miR-197-3p, YOD1 deubiquitinase (YOD1) and zinc finger protein 101 (ZNF101) and downstream connected genes was identified. Pathway enrichment analysis showed that DEmRNAs were enriched in “Protein processing in endoplasmic reticulum” and “Herpes simplex virus 1 infection” pathways. To our knowledge, this would be the first report of a possible role of SNHG1/hsa-miR-197-3p/YOD1/ZNF101 axes in the pathogenesis of MS. This research remarks on the significance of ceRNAs and prepares new perceptions for discovering the molecular mechanism of MS. Frontiers Media S.A. 2021-12-08 /pmc/articles/PMC8696673/ /pubmed/34956196 http://dx.doi.org/10.3389/fimmu.2021.770679 Text en Copyright © 2021 Sabaie, Salkhordeh, Asadi, Ghafouri-Fard, Amirinejad, Askarinejad Behzadi, Hussen, Taheri and Rezazadeh https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Sabaie, Hani
Salkhordeh, Zoha
Asadi, Mohammad Reza
Ghafouri-Fard, Soudeh
Amirinejad, Nazanin
Askarinejad Behzadi, Mahla
Hussen, Bashdar Mahmud
Taheri, Mohammad
Rezazadeh, Maryam
Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title_full Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title_fullStr Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title_full_unstemmed Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title_short Long Non-Coding RNA- Associated Competing Endogenous RNA Axes in T-Cells in Multiple Sclerosis
title_sort long non-coding rna- associated competing endogenous rna axes in t-cells in multiple sclerosis
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8696673/
https://www.ncbi.nlm.nih.gov/pubmed/34956196
http://dx.doi.org/10.3389/fimmu.2021.770679
work_keys_str_mv AT sabaiehani longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT salkhordehzoha longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT asadimohammadreza longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT ghafourifardsoudeh longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT amirinejadnazanin longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT askarinejadbehzadimahla longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT hussenbashdarmahmud longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT taherimohammad longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis
AT rezazadehmaryam longnoncodingrnaassociatedcompetingendogenousrnaaxesintcellsinmultiplesclerosis