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The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives
BACKGROUND: Salt-sensitivity hypertensives (SSH) are an independent risk factor for cardiovascular disease. However, the mechanism of SSH is not clear. This study is aimed at constructing a competing endogenous RNA (ceRNA) network related to SSH. METHODS: Data sets were collected from the Gene Expre...
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/PMC9586768/ https://www.ncbi.nlm.nih.gov/pubmed/36277897 http://dx.doi.org/10.1155/2022/8258351 |
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author | Liu, Xiu-Juan Yin, Hong-Lin Li, Yan Hao, Hao Liu, Yang Zhao, Quan-Lin |
author_facet | Liu, Xiu-Juan Yin, Hong-Lin Li, Yan Hao, Hao Liu, Yang Zhao, Quan-Lin |
author_sort | Liu, Xiu-Juan |
collection | PubMed |
description | BACKGROUND: Salt-sensitivity hypertensives (SSH) are an independent risk factor for cardiovascular disease. However, the mechanism of SSH is not clear. This study is aimed at constructing a competing endogenous RNA (ceRNA) network related to SSH. METHODS: Data sets were collected from the Gene Expression Omnibus database (GEO) to extract data on salt sensitivity RNA of patients with or without hypertensives in GSE135111. Firstly, we analyzed differentially expressed genes (DEGs, log2FC ≥ 0.5 and P < 0.05) and differentially expressed lncRNAs (DELs, log2FC ≥1 and P<0.05) between SSH and salt-sensitive normotension (SSN). Then, the gene ontology (GO), KEGG pathway enrichment analysis, and PPI network construction of DEGs were performed, and the hub genes in the PPI network by cytoHubba (12 methods) were screened out. Finally, a ceRNA network was constructed based on lncRNA-miRNA-mRNA pairs and hub genes. RESULTS: 163 DEGs and 65 DELs were screened out. The GO and KEGG pathway analyses of DEGs were mainly enriched in metabolism (e.g., insulin secretion and cellular response to glucagon stimulus and peptidyl-tyrosine dephosphorylation,) and plasma membrane signaling (e.g., cell adhesion and chemical synaptic transmission and integral component of membrane). Additionally, a ceRNA network, including 1 mRNA (EGLN3), 2 miRNAs (hsa-miR-17-5p and hsa-miR-20b-5p), and 1 lncRNA (C1orf143) was successfully constructed. CONCLUSIONS: In conclusion, the proposed ceRNA network may help elucidate the regulatory mechanism by which lncRNAs function as ceRNAs and contribute to the pathogenesis of SSH. Importantly, candidate lncRNAs, miRNAs, and mRNAs can be further evaluated as a potential therapeutic targets for SSH. |
format | Online Article Text |
id | pubmed-9586768 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-95867682022-10-22 The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives Liu, Xiu-Juan Yin, Hong-Lin Li, Yan Hao, Hao Liu, Yang Zhao, Quan-Lin Biomed Res Int Research Article BACKGROUND: Salt-sensitivity hypertensives (SSH) are an independent risk factor for cardiovascular disease. However, the mechanism of SSH is not clear. This study is aimed at constructing a competing endogenous RNA (ceRNA) network related to SSH. METHODS: Data sets were collected from the Gene Expression Omnibus database (GEO) to extract data on salt sensitivity RNA of patients with or without hypertensives in GSE135111. Firstly, we analyzed differentially expressed genes (DEGs, log2FC ≥ 0.5 and P < 0.05) and differentially expressed lncRNAs (DELs, log2FC ≥1 and P<0.05) between SSH and salt-sensitive normotension (SSN). Then, the gene ontology (GO), KEGG pathway enrichment analysis, and PPI network construction of DEGs were performed, and the hub genes in the PPI network by cytoHubba (12 methods) were screened out. Finally, a ceRNA network was constructed based on lncRNA-miRNA-mRNA pairs and hub genes. RESULTS: 163 DEGs and 65 DELs were screened out. The GO and KEGG pathway analyses of DEGs were mainly enriched in metabolism (e.g., insulin secretion and cellular response to glucagon stimulus and peptidyl-tyrosine dephosphorylation,) and plasma membrane signaling (e.g., cell adhesion and chemical synaptic transmission and integral component of membrane). Additionally, a ceRNA network, including 1 mRNA (EGLN3), 2 miRNAs (hsa-miR-17-5p and hsa-miR-20b-5p), and 1 lncRNA (C1orf143) was successfully constructed. CONCLUSIONS: In conclusion, the proposed ceRNA network may help elucidate the regulatory mechanism by which lncRNAs function as ceRNAs and contribute to the pathogenesis of SSH. Importantly, candidate lncRNAs, miRNAs, and mRNAs can be further evaluated as a potential therapeutic targets for SSH. Hindawi 2022-10-14 /pmc/articles/PMC9586768/ /pubmed/36277897 http://dx.doi.org/10.1155/2022/8258351 Text en Copyright © 2022 Xiu-Juan Liu 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 Liu, Xiu-Juan Yin, Hong-Lin Li, Yan Hao, Hao Liu, Yang Zhao, Quan-Lin The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title | The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title_full | The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title_fullStr | The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title_full_unstemmed | The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title_short | The Construction and Analysis of a ceRNA Network Related to Salt-Sensitivity Hypertensives |
title_sort | construction and analysis of a cerna network related to salt-sensitivity hypertensives |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9586768/ https://www.ncbi.nlm.nih.gov/pubmed/36277897 http://dx.doi.org/10.1155/2022/8258351 |
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