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Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus

Circular RNAs (circRNAs) constitute a class of covalently circular non-coding RNA molecules formed by 5′ and 3′ end back-splicing. The rapid development of bioinformatics and large-scale sequencing has led to the identification of functional circRNAs. Despite an overall upward trend, studies focusin...

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Autores principales: Yang, Lan, Han, Xiao, Zhang, Caiyan, Sun, Chengjun, Huang, Saihua, Xiao, Wenfeng, Gao, Yajing, Liang, Qiuyan, Luo, Feihong, Lu, Wei, Fu, Jinrong, Zhou, Yufeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7550460/
https://www.ncbi.nlm.nih.gov/pubmed/33133095
http://dx.doi.org/10.3389/fimmu.2020.576903
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author Yang, Lan
Han, Xiao
Zhang, Caiyan
Sun, Chengjun
Huang, Saihua
Xiao, Wenfeng
Gao, Yajing
Liang, Qiuyan
Luo, Feihong
Lu, Wei
Fu, Jinrong
Zhou, Yufeng
author_facet Yang, Lan
Han, Xiao
Zhang, Caiyan
Sun, Chengjun
Huang, Saihua
Xiao, Wenfeng
Gao, Yajing
Liang, Qiuyan
Luo, Feihong
Lu, Wei
Fu, Jinrong
Zhou, Yufeng
author_sort Yang, Lan
collection PubMed
description Circular RNAs (circRNAs) constitute a class of covalently circular non-coding RNA molecules formed by 5′ and 3′ end back-splicing. The rapid development of bioinformatics and large-scale sequencing has led to the identification of functional circRNAs. Despite an overall upward trend, studies focusing on the roles of circRNAs in immune diseases remain relatively scarce. In the present study, we obtained a differential circRNA expression profile based on microarray analysis of peripheral blood mononuclear cells (PBMCs) in children with type 1 diabetes mellitus (T1DM). We characterized one differentially expressed circRNA back-spliced from the MYB Proto-Oncogene Like 2 (MYBL2) gene in patients with T1DM, termed as hsa_circ_0060450. Subsequent assays revealed that hsa_circ_0060450 can serve as the sponge of miR-199a-5p, release its target gene, Src homology 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2), encoded by the tyrosine-protein phosphatase non-receptor type 11 gene (PTPN11), and further suppress the JAK-STAT signaling pathway triggered by type I interferon (IFN-I) to inhibit macrophage-mediated inflammation, which indicates the important roles of circRNAs in T1DM and represents a promising therapeutic molecule in the treatment of T1DM.
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spelling pubmed-75504602020-10-29 Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus Yang, Lan Han, Xiao Zhang, Caiyan Sun, Chengjun Huang, Saihua Xiao, Wenfeng Gao, Yajing Liang, Qiuyan Luo, Feihong Lu, Wei Fu, Jinrong Zhou, Yufeng Front Immunol Immunology Circular RNAs (circRNAs) constitute a class of covalently circular non-coding RNA molecules formed by 5′ and 3′ end back-splicing. The rapid development of bioinformatics and large-scale sequencing has led to the identification of functional circRNAs. Despite an overall upward trend, studies focusing on the roles of circRNAs in immune diseases remain relatively scarce. In the present study, we obtained a differential circRNA expression profile based on microarray analysis of peripheral blood mononuclear cells (PBMCs) in children with type 1 diabetes mellitus (T1DM). We characterized one differentially expressed circRNA back-spliced from the MYB Proto-Oncogene Like 2 (MYBL2) gene in patients with T1DM, termed as hsa_circ_0060450. Subsequent assays revealed that hsa_circ_0060450 can serve as the sponge of miR-199a-5p, release its target gene, Src homology 2 (SH2)-containing protein tyrosine phosphatase 2 (SHP2), encoded by the tyrosine-protein phosphatase non-receptor type 11 gene (PTPN11), and further suppress the JAK-STAT signaling pathway triggered by type I interferon (IFN-I) to inhibit macrophage-mediated inflammation, which indicates the important roles of circRNAs in T1DM and represents a promising therapeutic molecule in the treatment of T1DM. Frontiers Media S.A. 2020-09-29 /pmc/articles/PMC7550460/ /pubmed/33133095 http://dx.doi.org/10.3389/fimmu.2020.576903 Text en Copyright © 2020 Yang, Han, Zhang, Sun, Huang, Xiao, Gao, Liang, Luo, Lu, Fu and Zhou. http://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
Yang, Lan
Han, Xiao
Zhang, Caiyan
Sun, Chengjun
Huang, Saihua
Xiao, Wenfeng
Gao, Yajing
Liang, Qiuyan
Luo, Feihong
Lu, Wei
Fu, Jinrong
Zhou, Yufeng
Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title_full Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title_fullStr Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title_full_unstemmed Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title_short Hsa_circ_0060450 Negatively Regulates Type I Interferon-Induced Inflammation by Serving as miR-199a-5p Sponge in Type 1 Diabetes Mellitus
title_sort hsa_circ_0060450 negatively regulates type i interferon-induced inflammation by serving as mir-199a-5p sponge in type 1 diabetes mellitus
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7550460/
https://www.ncbi.nlm.nih.gov/pubmed/33133095
http://dx.doi.org/10.3389/fimmu.2020.576903
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