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Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1
Acute myocardial infarction (AMI) is a complication of atherosclerosis-related cardiovascular illness that is caused by prolonged ischemia. Circular RNAs (circRNAs) are concentrated in extracellular vesicles (EVs) and have been linked to cardiovascular disease. However, additional research is needed...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9126660/ https://www.ncbi.nlm.nih.gov/pubmed/35615580 http://dx.doi.org/10.1155/2022/8392313 |
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author | Zhu, Jianbing Chen, Zhaoyang Peng, Xiaoping Zheng, Zeqi Le, Aiping Guo, Junjie Ma, Leilei Shi, Hongtao Yao, Kang Zhang, Shuning Ge, Junbo Zheng, Zhenzhong Wang, Qian |
author_facet | Zhu, Jianbing Chen, Zhaoyang Peng, Xiaoping Zheng, Zeqi Le, Aiping Guo, Junjie Ma, Leilei Shi, Hongtao Yao, Kang Zhang, Shuning Ge, Junbo Zheng, Zhenzhong Wang, Qian |
author_sort | Zhu, Jianbing |
collection | PubMed |
description | Acute myocardial infarction (AMI) is a complication of atherosclerosis-related cardiovascular illness that is caused by prolonged ischemia. Circular RNAs (circRNAs) are concentrated in extracellular vesicles (EVs) and have been linked to cardiovascular disease. However, additional research is needed into the expression and function of circRNAs in AMI. In this study, circITGB1 (has_circRNA_0018146), derived from exon 1 of the ITGB1 gene localized on chromosome 10, was shown to be considerably increased in plasma from patients with AMI compared to healthy controls, as demonstrated by the comparison of EV-circRNA expression patterns. Using a luciferase screening assay and a biotin-labeled circITGB1 probe to identify microRNA(s) complementary to circITGB1 sequences, we discovered that circITGB1 competitively binds to miR-342-3p and inhibits its expression, which in turn increase the expression of NFAT activating molecule 1 (NFAM1). Based on western blotting and immunological studies, circITGB1 controls dendritic cell maturation by targeting miR-342-3p and NFAM1. circITGB1 also exacerbated cardiac damage and regulated miR-342-3p and NFAM1 expression in a mouse AMI model. This implies that EV-circITGB1 is involved in dendritic cell maturation and cardiac damage via miR-342-3p/NFAM1, and that is linked to AMI-associated pathogenic processes. |
format | Online Article Text |
id | pubmed-9126660 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-91266602022-05-24 Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 Zhu, Jianbing Chen, Zhaoyang Peng, Xiaoping Zheng, Zeqi Le, Aiping Guo, Junjie Ma, Leilei Shi, Hongtao Yao, Kang Zhang, Shuning Ge, Junbo Zheng, Zhenzhong Wang, Qian Oxid Med Cell Longev Research Article Acute myocardial infarction (AMI) is a complication of atherosclerosis-related cardiovascular illness that is caused by prolonged ischemia. Circular RNAs (circRNAs) are concentrated in extracellular vesicles (EVs) and have been linked to cardiovascular disease. However, additional research is needed into the expression and function of circRNAs in AMI. In this study, circITGB1 (has_circRNA_0018146), derived from exon 1 of the ITGB1 gene localized on chromosome 10, was shown to be considerably increased in plasma from patients with AMI compared to healthy controls, as demonstrated by the comparison of EV-circRNA expression patterns. Using a luciferase screening assay and a biotin-labeled circITGB1 probe to identify microRNA(s) complementary to circITGB1 sequences, we discovered that circITGB1 competitively binds to miR-342-3p and inhibits its expression, which in turn increase the expression of NFAT activating molecule 1 (NFAM1). Based on western blotting and immunological studies, circITGB1 controls dendritic cell maturation by targeting miR-342-3p and NFAM1. circITGB1 also exacerbated cardiac damage and regulated miR-342-3p and NFAM1 expression in a mouse AMI model. This implies that EV-circITGB1 is involved in dendritic cell maturation and cardiac damage via miR-342-3p/NFAM1, and that is linked to AMI-associated pathogenic processes. Hindawi 2022-05-16 /pmc/articles/PMC9126660/ /pubmed/35615580 http://dx.doi.org/10.1155/2022/8392313 Text en Copyright © 2022 Jianbing Zhu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhu, Jianbing Chen, Zhaoyang Peng, Xiaoping Zheng, Zeqi Le, Aiping Guo, Junjie Ma, Leilei Shi, Hongtao Yao, Kang Zhang, Shuning Ge, Junbo Zheng, Zhenzhong Wang, Qian Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title | Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title_full | Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title_fullStr | Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title_full_unstemmed | Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title_short | Extracellular Vesicle-Derived circITGB1 Regulates Dendritic Cell Maturation and Cardiac Inflammation via miR-342-3p/NFAM1 |
title_sort | extracellular vesicle-derived circitgb1 regulates dendritic cell maturation and cardiac inflammation via mir-342-3p/nfam1 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9126660/ https://www.ncbi.nlm.nih.gov/pubmed/35615580 http://dx.doi.org/10.1155/2022/8392313 |
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