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Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome
Idiopathic pulmonary fibrosis (IPF) is an age-related interstitial lung disease with a high incidence in the elderly. Although many reports have shown that senescence can initiate pulmonary fibrosis, the relationship between aging and pulmonary fibrosis has not been explained systematically. In our...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9788318/ https://www.ncbi.nlm.nih.gov/pubmed/36556326 http://dx.doi.org/10.3390/life12121961 |
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author | Fu, San Tang, Xiaoyan Xu, Yiming Song, Xianrui Qian, Xiuhui Hu, Yingying Zhang, Mian |
author_facet | Fu, San Tang, Xiaoyan Xu, Yiming Song, Xianrui Qian, Xiuhui Hu, Yingying Zhang, Mian |
author_sort | Fu, San |
collection | PubMed |
description | Idiopathic pulmonary fibrosis (IPF) is an age-related interstitial lung disease with a high incidence in the elderly. Although many reports have shown that senescence can initiate pulmonary fibrosis, the relationship between aging and pulmonary fibrosis has not been explained systematically. In our study, young and old rats were intratracheally instilled with bleomycin (1 mg/kg), and the basic pathological indexes were determined using a commercial kit, hematoxylin, and eosin (H&E) and Masson’s Trichrome staining, immunohistochemistry, immunohistofluorescence, and q-PCR. Then, the lung tissues of rats were sequenced by next-generation sequencing for transcriptome analysis. Bioinformatics was performed to analyze the possible differences in the mechanism of pulmonary fibrosis between aged and young rats. Finally, the related cytokines were determined by q-PCR and ELISA. The results indicate that pulmonary fibrosis in old rats is more serious than that in young rats under the same conditions. Additionally, transcriptomic and bioinformatics analysis with experimental validation indicate that the differences in pulmonary fibrosis between old and young rats are mainly related to the differential expression of cytokines, extracellular matrix (ECM), and other important signaling pathways. In conclusion, aging mainly affects pulmonary fibrosis through the ECM–receptor interaction, immune response, and chemokines. |
format | Online Article Text |
id | pubmed-9788318 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-97883182022-12-24 Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome Fu, San Tang, Xiaoyan Xu, Yiming Song, Xianrui Qian, Xiuhui Hu, Yingying Zhang, Mian Life (Basel) Article Idiopathic pulmonary fibrosis (IPF) is an age-related interstitial lung disease with a high incidence in the elderly. Although many reports have shown that senescence can initiate pulmonary fibrosis, the relationship between aging and pulmonary fibrosis has not been explained systematically. In our study, young and old rats were intratracheally instilled with bleomycin (1 mg/kg), and the basic pathological indexes were determined using a commercial kit, hematoxylin, and eosin (H&E) and Masson’s Trichrome staining, immunohistochemistry, immunohistofluorescence, and q-PCR. Then, the lung tissues of rats were sequenced by next-generation sequencing for transcriptome analysis. Bioinformatics was performed to analyze the possible differences in the mechanism of pulmonary fibrosis between aged and young rats. Finally, the related cytokines were determined by q-PCR and ELISA. The results indicate that pulmonary fibrosis in old rats is more serious than that in young rats under the same conditions. Additionally, transcriptomic and bioinformatics analysis with experimental validation indicate that the differences in pulmonary fibrosis between old and young rats are mainly related to the differential expression of cytokines, extracellular matrix (ECM), and other important signaling pathways. In conclusion, aging mainly affects pulmonary fibrosis through the ECM–receptor interaction, immune response, and chemokines. MDPI 2022-11-23 /pmc/articles/PMC9788318/ /pubmed/36556326 http://dx.doi.org/10.3390/life12121961 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Fu, San Tang, Xiaoyan Xu, Yiming Song, Xianrui Qian, Xiuhui Hu, Yingying Zhang, Mian Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title | Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title_full | Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title_fullStr | Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title_full_unstemmed | Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title_short | Analysis of the Potential Relationship between Aging and Pulmonary Fibrosis Based on Transcriptome |
title_sort | analysis of the potential relationship between aging and pulmonary fibrosis based on transcriptome |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9788318/ https://www.ncbi.nlm.nih.gov/pubmed/36556326 http://dx.doi.org/10.3390/life12121961 |
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