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CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease
Increasing evidence suggests that circular RNAs (circRNAs) play critical roles in various pathophysiological activities. However, the role of circRNAs in inflammatory bowel disease (IBD) remains unclear. Here we report the potential roles of hsa_circRNA_103765 in regulating cell apoptosis induced by...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804428/ https://www.ncbi.nlm.nih.gov/pubmed/33436852 http://dx.doi.org/10.1038/s41598-020-80663-w |
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author | Ye, Yulan Zhang, Liping Hu, Tong Yin, Juan Xu, Lijuan Pang, Zhi Chen, Weichang |
author_facet | Ye, Yulan Zhang, Liping Hu, Tong Yin, Juan Xu, Lijuan Pang, Zhi Chen, Weichang |
author_sort | Ye, Yulan |
collection | PubMed |
description | Increasing evidence suggests that circular RNAs (circRNAs) play critical roles in various pathophysiological activities. However, the role of circRNAs in inflammatory bowel disease (IBD) remains unclear. Here we report the potential roles of hsa_circRNA_103765 in regulating cell apoptosis induced by TNF-α in Crohn’s disease (CD). We identify that CircRNA_103765 expression was significantly upregulated in peripheral blood mononuclear cells (PBMCs) of patients with active IBD. A positive correlation with TNF-α significantly enhanced circRNA_103765 expression in CD, which was significantly reversed by anti-TNF-α mAb (infliximab) treatment. In vitro experiments showed that TNF-α could induce the expression of circRNA_103765, which was cell apoptosis dependent, while silencing of circRNA_103765 could protect human intestinal epithelial cells (IECs) from TNF-α-induced apoptosis. In addition, circRNA_103765 acted as a molecular sponge to adsorb the miR-30 family and impair the negative regulation of Delta-like ligand 4 (DLL4). Collectively, CircRNA_103765 is a novel important regulator of the pathogenesis of IBD via sponging miR-30 family-mediated DLL4 expression changes. Blockade of circRNA_103765 could serve as a novel approach for the treatment of IBD patients. |
format | Online Article Text |
id | pubmed-7804428 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-78044282021-01-13 CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease Ye, Yulan Zhang, Liping Hu, Tong Yin, Juan Xu, Lijuan Pang, Zhi Chen, Weichang Sci Rep Article Increasing evidence suggests that circular RNAs (circRNAs) play critical roles in various pathophysiological activities. However, the role of circRNAs in inflammatory bowel disease (IBD) remains unclear. Here we report the potential roles of hsa_circRNA_103765 in regulating cell apoptosis induced by TNF-α in Crohn’s disease (CD). We identify that CircRNA_103765 expression was significantly upregulated in peripheral blood mononuclear cells (PBMCs) of patients with active IBD. A positive correlation with TNF-α significantly enhanced circRNA_103765 expression in CD, which was significantly reversed by anti-TNF-α mAb (infliximab) treatment. In vitro experiments showed that TNF-α could induce the expression of circRNA_103765, which was cell apoptosis dependent, while silencing of circRNA_103765 could protect human intestinal epithelial cells (IECs) from TNF-α-induced apoptosis. In addition, circRNA_103765 acted as a molecular sponge to adsorb the miR-30 family and impair the negative regulation of Delta-like ligand 4 (DLL4). Collectively, CircRNA_103765 is a novel important regulator of the pathogenesis of IBD via sponging miR-30 family-mediated DLL4 expression changes. Blockade of circRNA_103765 could serve as a novel approach for the treatment of IBD patients. Nature Publishing Group UK 2021-01-12 /pmc/articles/PMC7804428/ /pubmed/33436852 http://dx.doi.org/10.1038/s41598-020-80663-w Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Ye, Yulan Zhang, Liping Hu, Tong Yin, Juan Xu, Lijuan Pang, Zhi Chen, Weichang CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title | CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title_full | CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title_fullStr | CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title_full_unstemmed | CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title_short | CircRNA_103765 acts as a proinflammatory factor via sponging miR-30 family in Crohn’s disease |
title_sort | circrna_103765 acts as a proinflammatory factor via sponging mir-30 family in crohn’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7804428/ https://www.ncbi.nlm.nih.gov/pubmed/33436852 http://dx.doi.org/10.1038/s41598-020-80663-w |
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