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CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation
Atrial fibrillation (AF) is a rapid supraventricular arrhythmia. However, the pathogenesis of atrial fibrillation remains controversial. We obtained transcriptome expression profiles GSE41177, GSE115574 and GSE79768 from GEO database. WGCNA was performed, DEGs were screened, PPI network was construc...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9189330/ https://www.ncbi.nlm.nih.gov/pubmed/35607269 http://dx.doi.org/10.1111/jcmm.17405 |
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author | Zhang, Yan‐Fei Meng, Ling‐Bing Hao, Meng‐Lei Li, Xing‐Yu Zou, Tong |
author_facet | Zhang, Yan‐Fei Meng, Ling‐Bing Hao, Meng‐Lei Li, Xing‐Yu Zou, Tong |
author_sort | Zhang, Yan‐Fei |
collection | PubMed |
description | Atrial fibrillation (AF) is a rapid supraventricular arrhythmia. However, the pathogenesis of atrial fibrillation remains controversial. We obtained transcriptome expression profiles GSE41177, GSE115574 and GSE79768 from GEO database. WGCNA was performed, DEGs were screened, PPI network was constructed using STRING database. CTD database was used to identify the reference score of hub genes associated with cardiovascular diseases. Prediction of miRNAs of hub genes was performed by TargetScan. DIANA‐miRPath v3.0 was applied to make functional annotation of miRNA. The animal model of atrial fibrillation was constructed, RT‐PCR was used to verify the expression of hub genes. Immunofluorescence assay for THBS2 and VCAN was made to identify molecular. Design of BP neural network was made to explore the prediction relationship of CXCR4 and TYROBP on AF. The merged datasets contained 104 up‐regulated and 34 down‐regulated genes. GO and KEGG enrichment analysis results of DEGs showed they were mainly enriched in ‘regulation of release of sequestered calcium ion into cytosol’, ‘actin cytoskeleton organization’ and ‘focal adhesion’. The hub genes were CXCR4, SNAI2, S100A4, IGFBP3, CSNK2A1, CHGB, VCAN, APOE, C1QC and TYROBP, which were up‐regulated expression in the AF compared with control tissues. There was strong correlation among the CXCR4, TYROBP and AF based on the BP neural network. Through training, best training performance is 9.6474e‐05 at epoch 14, and the relativity was 0.99998. CXCR4 and TYROBP might be involved in the development of atrial fibrillation by affecting inflammation‐related signalling pathways and may serve as targets for early diagnosis and preventive treatment. |
format | Online Article Text |
id | pubmed-9189330 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-91893302022-06-16 CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation Zhang, Yan‐Fei Meng, Ling‐Bing Hao, Meng‐Lei Li, Xing‐Yu Zou, Tong J Cell Mol Med Original Articles Atrial fibrillation (AF) is a rapid supraventricular arrhythmia. However, the pathogenesis of atrial fibrillation remains controversial. We obtained transcriptome expression profiles GSE41177, GSE115574 and GSE79768 from GEO database. WGCNA was performed, DEGs were screened, PPI network was constructed using STRING database. CTD database was used to identify the reference score of hub genes associated with cardiovascular diseases. Prediction of miRNAs of hub genes was performed by TargetScan. DIANA‐miRPath v3.0 was applied to make functional annotation of miRNA. The animal model of atrial fibrillation was constructed, RT‐PCR was used to verify the expression of hub genes. Immunofluorescence assay for THBS2 and VCAN was made to identify molecular. Design of BP neural network was made to explore the prediction relationship of CXCR4 and TYROBP on AF. The merged datasets contained 104 up‐regulated and 34 down‐regulated genes. GO and KEGG enrichment analysis results of DEGs showed they were mainly enriched in ‘regulation of release of sequestered calcium ion into cytosol’, ‘actin cytoskeleton organization’ and ‘focal adhesion’. The hub genes were CXCR4, SNAI2, S100A4, IGFBP3, CSNK2A1, CHGB, VCAN, APOE, C1QC and TYROBP, which were up‐regulated expression in the AF compared with control tissues. There was strong correlation among the CXCR4, TYROBP and AF based on the BP neural network. Through training, best training performance is 9.6474e‐05 at epoch 14, and the relativity was 0.99998. CXCR4 and TYROBP might be involved in the development of atrial fibrillation by affecting inflammation‐related signalling pathways and may serve as targets for early diagnosis and preventive treatment. John Wiley and Sons Inc. 2022-05-23 2022-06 /pmc/articles/PMC9189330/ /pubmed/35607269 http://dx.doi.org/10.1111/jcmm.17405 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Zhang, Yan‐Fei Meng, Ling‐Bing Hao, Meng‐Lei Li, Xing‐Yu Zou, Tong CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title |
CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title_full |
CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title_fullStr |
CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title_full_unstemmed |
CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title_short |
CXCR4 and TYROBP mediate the development of atrial fibrillation via inflammation |
title_sort | cxcr4 and tyrobp mediate the development of atrial fibrillation via inflammation |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9189330/ https://www.ncbi.nlm.nih.gov/pubmed/35607269 http://dx.doi.org/10.1111/jcmm.17405 |
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