MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation

Objective(s): Multiple sclerosis (MS) is considered as a chronic type of an inflammatory disease characterized by loss of myelin of CNS.Recent evidence indicates that Interleukin 17 (IL-17)-producing T helper cells (Th17 cells) population are increased and regulatory T cells (Treg cells) are decreas...

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Main Authors: Maryam Majd, Aref Hosseini, Kamran Ghaedi, Abbas Kiani-Esfahani, Somayeh Tanhaei, Hanieh Shiralian-Esfahani, Seyed Yahya Rahnamaee, Seyed Javad Mowla, Mohamad Hosein Nasr Esfahani
Format: Article
Language:English
Published: Mashhad University of Medical Sciences 2018-03-01
Series:Iranian Journal of Basic Medical Sciences
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Online Access:http://ijbms.mums.ac.ir/article_10198_08cb84014acd2b7af4614a6b6a02134d.pdf
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author Maryam Majd
Aref Hosseini
Kamran Ghaedi
Abbas Kiani-Esfahani
Somayeh Tanhaei
Hanieh Shiralian-Esfahani
Seyed Yahya Rahnamaee
Seyed Javad Mowla
Mohamad Hosein Nasr Esfahani
author_facet Maryam Majd
Aref Hosseini
Kamran Ghaedi
Abbas Kiani-Esfahani
Somayeh Tanhaei
Hanieh Shiralian-Esfahani
Seyed Yahya Rahnamaee
Seyed Javad Mowla
Mohamad Hosein Nasr Esfahani
author_sort Maryam Majd
collection DOAJ
description Objective(s): Multiple sclerosis (MS) is considered as a chronic type of an inflammatory disease characterized by loss of myelin of CNS.Recent evidence indicates that Interleukin 17 (IL-17)-producing T helper cells (Th17 cells) population are increased and regulatory T cells (Treg cells) are decreased in MS. Despite extensive research in understanding the mechanism of Th17 and Treg differentiation, the role of microRNAs in MS is not completely understood. Thereby, as a step closer, we analyzed the expression profile of miR-9-5p and miR-106a-5p, and protein level of retinoic acid receptor (RAR)-related orphan receptor C (RORC; Th17 master transcription factor) as direct target of miR-106a-5p and forkhead box P3 (FOXP3; Treg master transcription factor) as indirect target of miR-9-5p in CD4+ T cells in two groups of relapsing and remitting in our relapsing-remitting MS (RR-MS) patients. Materials and Methods:Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was utilized to assess the expression of miRNAs and mRNAs, in 40 RR-MS patients and 11 healthy individuals. Thus, FOXP3 and RAR-related orphan receptor γt (RORγt) was assessed in CD4+T-cells by flow cytometry. We also investigated the role of these miRNAs in Th17/Treg differentiation pathway through bioinformatics tools. Results: An up-regulation of miR-9-5p and down-regulation of miR-106a-5p in relapsing phase of MS patients were observed compared to healthy controls. RORC and FOXP3 wereup-regulated in relapsing and remitting phases of MS, respectively. Conclusion: Expression pattern of miR-9-5p and miR-106a-5p and their targets suggest a possible inducing role of miR-9-5p and suppressing role of miR-106a-5p in differentiation pathway of Th17 cells during MS pathogenesis.
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spelling doaj.art-d9f04ed32a034ed488693acd6c3ccfe82022-12-22T00:26:20ZengMashhad University of Medical SciencesIranian Journal of Basic Medical Sciences2008-38662008-38742018-03-0121327728310.22038/ijbms.2018.25382.627510198MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiationMaryam Majd0Aref Hosseini1Kamran Ghaedi2Abbas Kiani-Esfahani3Somayeh Tanhaei4Hanieh Shiralian-Esfahani5Seyed Yahya Rahnamaee6Seyed Javad Mowla7Mohamad Hosein Nasr Esfahani8Molecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, IranDivision of Cellular and Molecular Biology, Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran|Department of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranDivision of Cellular and Molecular Biology, Department of Biology, Faculty of Sciences, University of Isfahan, Isfahan, Iran|Department of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranInstitute for Nanoscience and Nanotechnology, Sharif University of Technology, Tehran, IranMolecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, IranDepartment of Cellular Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, IranObjective(s): Multiple sclerosis (MS) is considered as a chronic type of an inflammatory disease characterized by loss of myelin of CNS.Recent evidence indicates that Interleukin 17 (IL-17)-producing T helper cells (Th17 cells) population are increased and regulatory T cells (Treg cells) are decreased in MS. Despite extensive research in understanding the mechanism of Th17 and Treg differentiation, the role of microRNAs in MS is not completely understood. Thereby, as a step closer, we analyzed the expression profile of miR-9-5p and miR-106a-5p, and protein level of retinoic acid receptor (RAR)-related orphan receptor C (RORC; Th17 master transcription factor) as direct target of miR-106a-5p and forkhead box P3 (FOXP3; Treg master transcription factor) as indirect target of miR-9-5p in CD4+ T cells in two groups of relapsing and remitting in our relapsing-remitting MS (RR-MS) patients. Materials and Methods:Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was utilized to assess the expression of miRNAs and mRNAs, in 40 RR-MS patients and 11 healthy individuals. Thus, FOXP3 and RAR-related orphan receptor γt (RORγt) was assessed in CD4+T-cells by flow cytometry. We also investigated the role of these miRNAs in Th17/Treg differentiation pathway through bioinformatics tools. Results: An up-regulation of miR-9-5p and down-regulation of miR-106a-5p in relapsing phase of MS patients were observed compared to healthy controls. RORC and FOXP3 wereup-regulated in relapsing and remitting phases of MS, respectively. Conclusion: Expression pattern of miR-9-5p and miR-106a-5p and their targets suggest a possible inducing role of miR-9-5p and suppressing role of miR-106a-5p in differentiation pathway of Th17 cells during MS pathogenesis.http://ijbms.mums.ac.ir/article_10198_08cb84014acd2b7af4614a6b6a02134d.pdfMicroRNAMiR-106a-5pMiR-9-5pMultiple sclerosisTh17
spellingShingle Maryam Majd
Aref Hosseini
Kamran Ghaedi
Abbas Kiani-Esfahani
Somayeh Tanhaei
Hanieh Shiralian-Esfahani
Seyed Yahya Rahnamaee
Seyed Javad Mowla
Mohamad Hosein Nasr Esfahani
MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
Iranian Journal of Basic Medical Sciences
MicroRNA
MiR-106a-5p
MiR-9-5p
Multiple sclerosis
Th17
title MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
title_full MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
title_fullStr MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
title_full_unstemmed MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
title_short MiR-9-5p and miR-106a-5p dysregulated in CD4+ T-cells of multiple sclerosis patients and targeted essential factors of T helper17/regulatory T-cells differentiation
title_sort mir 9 5p and mir 106a 5p dysregulated in cd4 t cells of multiple sclerosis patients and targeted essential factors of t helper17 regulatory t cells differentiation
topic MicroRNA
MiR-106a-5p
MiR-9-5p
Multiple sclerosis
Th17
url http://ijbms.mums.ac.ir/article_10198_08cb84014acd2b7af4614a6b6a02134d.pdf
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