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Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model
Radiation-induced lung injury (RILI) can be challenging for thoracic radiotherapy, thus investigating its mechanisms of related pathophysiological process is needed. Long noncoding RNAs (lncRNAs) was found to participate in normal tissue damage induced by ionizing irradiation. Here, we first profile...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6909272/ https://www.ncbi.nlm.nih.gov/pubmed/31853236 http://dx.doi.org/10.1177/1559325819891012 |
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author | Li, Yida Zou, Liqing Yang, Xi Chu, Li Ni, Jianjiao Chu, Xiao Guo, Tiantian Zhu, Zhengfei |
author_facet | Li, Yida Zou, Liqing Yang, Xi Chu, Li Ni, Jianjiao Chu, Xiao Guo, Tiantian Zhu, Zhengfei |
author_sort | Li, Yida |
collection | PubMed |
description | Radiation-induced lung injury (RILI) can be challenging for thoracic radiotherapy, thus investigating its mechanisms of related pathophysiological process is needed. Long noncoding RNAs (lncRNAs) was found to participate in normal tissue damage induced by ionizing irradiation. Here, we first profiled the dysregulation of lncRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) of RILI in mice model receiving 12 Gy thoracic irradiation. The lung tissue was collected 48 hours after irradiation, after which an RNA library was built by RNA sequencing. Compared with the control group, 461 mRNAs and 401 lncRNAs were significantly upregulated, while 936 mRNAs and 501 lncRNAs were significantly downregulated. Then we predicted target miRNAs of the dysregulated lncRNAs and the target mRNAs of these miRNAs. Next, functional annotations of these target mRNAs were performed. Results showed some pathways apparently dysregulated, such as Th1 and Th2 cell differentiation, Th17 cell differentiation, and hematopoietic cell lineage. Through this study, we also highlighted that T helpers could be vital in RILI through lncRNA-miRNA-mRNA network, therefore causing fibrosis, indicating that RNA dysregulation in early stage of RILI may cause severe late complications. Thus, research on the target mechanism and early intervention of lncRNAs with associated competing endogenous RNA network will benefit the treatment of RILI. |
format | Online Article Text |
id | pubmed-6909272 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-69092722019-12-18 Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model Li, Yida Zou, Liqing Yang, Xi Chu, Li Ni, Jianjiao Chu, Xiao Guo, Tiantian Zhu, Zhengfei Dose Response Original Article Radiation-induced lung injury (RILI) can be challenging for thoracic radiotherapy, thus investigating its mechanisms of related pathophysiological process is needed. Long noncoding RNAs (lncRNAs) was found to participate in normal tissue damage induced by ionizing irradiation. Here, we first profiled the dysregulation of lncRNAs, microRNAs (miRNAs), and messenger RNAs (mRNAs) of RILI in mice model receiving 12 Gy thoracic irradiation. The lung tissue was collected 48 hours after irradiation, after which an RNA library was built by RNA sequencing. Compared with the control group, 461 mRNAs and 401 lncRNAs were significantly upregulated, while 936 mRNAs and 501 lncRNAs were significantly downregulated. Then we predicted target miRNAs of the dysregulated lncRNAs and the target mRNAs of these miRNAs. Next, functional annotations of these target mRNAs were performed. Results showed some pathways apparently dysregulated, such as Th1 and Th2 cell differentiation, Th17 cell differentiation, and hematopoietic cell lineage. Through this study, we also highlighted that T helpers could be vital in RILI through lncRNA-miRNA-mRNA network, therefore causing fibrosis, indicating that RNA dysregulation in early stage of RILI may cause severe late complications. Thus, research on the target mechanism and early intervention of lncRNAs with associated competing endogenous RNA network will benefit the treatment of RILI. SAGE Publications 2019-12-12 /pmc/articles/PMC6909272/ /pubmed/31853236 http://dx.doi.org/10.1177/1559325819891012 Text en © The Author(s) 2019 http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Article Li, Yida Zou, Liqing Yang, Xi Chu, Li Ni, Jianjiao Chu, Xiao Guo, Tiantian Zhu, Zhengfei Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title | Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title_full | Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title_fullStr | Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title_full_unstemmed | Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title_short | Identification of lncRNA, MicroRNA, and mRNA-Associated CeRNA Network of Radiation-Induced Lung Injury in a Mice Model |
title_sort | identification of lncrna, microrna, and mrna-associated cerna network of radiation-induced lung injury in a mice model |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6909272/ https://www.ncbi.nlm.nih.gov/pubmed/31853236 http://dx.doi.org/10.1177/1559325819891012 |
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