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Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers
BACKGROUND: Emerging evidence shows that exosomes play a crucial role in the occurrence and development of diabetes and its complications. The molecules in exosomes can be regarded as important markers for the diagnosis of diseases. However, it is presently unclear the pathological association mecha...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9682028/ https://www.ncbi.nlm.nih.gov/pubmed/36440209 http://dx.doi.org/10.3389/fendo.2022.1015800 |
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author | Fang, Tian Xue, Gong Jianjun, Wu Wei, Long Xiaomeng, Zhang Fan, Yang |
author_facet | Fang, Tian Xue, Gong Jianjun, Wu Wei, Long Xiaomeng, Zhang Fan, Yang |
author_sort | Fang, Tian |
collection | PubMed |
description | BACKGROUND: Emerging evidence shows that exosomes play a crucial role in the occurrence and development of diabetes and its complications. The molecules in exosomes can be regarded as important markers for the diagnosis of diseases. However, it is presently unclear the pathological association mechanism between exosomes and diabetes. RESULTS: In this study, transcriptome data and lncRNA regulatory association data of human pancreatic islet-derived exosome were integrated to construct the ceRNA network. Network analysis revealed that lncRNA with differential expression were primarily involved in islet insulin secretion signaling pathways, including Hippo, TGF-beta, Wnt, FOXO, Neurotrophin and ErbB signaling pathway. Further, combined with miRNA mediated competitive regulation and differential expression analysis results, potential markers of diabetes were revealed and validated in independent datasets. Finally, we analyzed the mechanisms of diabetes based on the competitive regulatory association and function of lncRNA. CONCLUSION: Our results suggest that lncRNA such as lncRNA PVT1, LINC00960 and hsa-miR-107 might be involved in inflammation response in T1DM, and the former lncRNA chose in the present study may serve as novel biomarkers and potential targets for the diagnosis and treatment of T1DM. |
format | Online Article Text |
id | pubmed-9682028 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-96820282022-11-24 Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers Fang, Tian Xue, Gong Jianjun, Wu Wei, Long Xiaomeng, Zhang Fan, Yang Front Endocrinol (Lausanne) Endocrinology BACKGROUND: Emerging evidence shows that exosomes play a crucial role in the occurrence and development of diabetes and its complications. The molecules in exosomes can be regarded as important markers for the diagnosis of diseases. However, it is presently unclear the pathological association mechanism between exosomes and diabetes. RESULTS: In this study, transcriptome data and lncRNA regulatory association data of human pancreatic islet-derived exosome were integrated to construct the ceRNA network. Network analysis revealed that lncRNA with differential expression were primarily involved in islet insulin secretion signaling pathways, including Hippo, TGF-beta, Wnt, FOXO, Neurotrophin and ErbB signaling pathway. Further, combined with miRNA mediated competitive regulation and differential expression analysis results, potential markers of diabetes were revealed and validated in independent datasets. Finally, we analyzed the mechanisms of diabetes based on the competitive regulatory association and function of lncRNA. CONCLUSION: Our results suggest that lncRNA such as lncRNA PVT1, LINC00960 and hsa-miR-107 might be involved in inflammation response in T1DM, and the former lncRNA chose in the present study may serve as novel biomarkers and potential targets for the diagnosis and treatment of T1DM. Frontiers Media S.A. 2022-11-09 /pmc/articles/PMC9682028/ /pubmed/36440209 http://dx.doi.org/10.3389/fendo.2022.1015800 Text en Copyright © 2022 Fang, Xue, Jianjun, Wei, Xiaomeng and Fan 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 | Endocrinology Fang, Tian Xue, Gong Jianjun, Wu Wei, Long Xiaomeng, Zhang Fan, Yang Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title | Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title_full | Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title_fullStr | Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title_full_unstemmed | Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title_short | Dissecting lncRNA-mRNA competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome miRNA markers |
title_sort | dissecting lncrna-mrna competitive regulatory network in human islet tissue exosomes of a type 1 diabetes model reveals exosome mirna markers |
topic | Endocrinology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9682028/ https://www.ncbi.nlm.nih.gov/pubmed/36440209 http://dx.doi.org/10.3389/fendo.2022.1015800 |
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