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Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development

BACKGROUND: Foam cells (FCs) play crucial roles in the process of all stages of atherosclerosis. Smooth muscle cells (SMCs) and macrophages are the major sources of FCs. This study aimed to identify the common molecular mechanism in these two types of FCs. METHODS: GSE28829, GSE43292, GSE68021, and...

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Autores principales: Zhang, Kai, Qin, Xianyu, Zhou, Xianwu, Zhou, Jianrong, Wen, Pengju, Chen, Shaoxian, Wu, Min, Wu, Yueheng, Zhuang, Jian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7678445/
https://www.ncbi.nlm.nih.gov/pubmed/33240650
http://dx.doi.org/10.7717/peerj.10336
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author Zhang, Kai
Qin, Xianyu
Zhou, Xianwu
Zhou, Jianrong
Wen, Pengju
Chen, Shaoxian
Wu, Min
Wu, Yueheng
Zhuang, Jian
author_facet Zhang, Kai
Qin, Xianyu
Zhou, Xianwu
Zhou, Jianrong
Wen, Pengju
Chen, Shaoxian
Wu, Min
Wu, Yueheng
Zhuang, Jian
author_sort Zhang, Kai
collection PubMed
description BACKGROUND: Foam cells (FCs) play crucial roles in the process of all stages of atherosclerosis. Smooth muscle cells (SMCs) and macrophages are the major sources of FCs. This study aimed to identify the common molecular mechanism in these two types of FCs. METHODS: GSE28829, GSE43292, GSE68021, and GSE54666 were included to identify the differentially expressed genes (DEGs) associated with FCs derived from SMCs and macrophages. Gene Ontology biological process (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed by using the DAVID database. The co-regulated genes associated with the two origins of FCs were validated (GSE9874), and their expression in vulnerable atherosclerosis plaques (GSE120521 and GSE41571) was assessed. RESULTS: A total of 432 genes associated with FCs derived from SMCs (SMC-FCs) and 81 genes associated with FCs derived from macrophages (M-FCs) were identified, and they were mainly involved in lipid metabolism, inflammation, cell cycle/apoptosis. Furthermore, three co-regulated genes associated with FCs were identified: GLRX, RNF13, and ABCA1. These three common genes showed an increased tendency in unstable or ruptured plaques, although in some cases, no statistically significant difference was found. CONCLUSIONS: DEGs related to FCs derived from SMCs and macrophages have contributed to the understanding of the molecular mechanism underlying the formation of FCs and atherosclerosis. GLRX, RNF13, and ABCA1 might be potential targets for atherosclerosis treatment.
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spelling pubmed-76784452020-11-24 Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development Zhang, Kai Qin, Xianyu Zhou, Xianwu Zhou, Jianrong Wen, Pengju Chen, Shaoxian Wu, Min Wu, Yueheng Zhuang, Jian PeerJ Bioinformatics BACKGROUND: Foam cells (FCs) play crucial roles in the process of all stages of atherosclerosis. Smooth muscle cells (SMCs) and macrophages are the major sources of FCs. This study aimed to identify the common molecular mechanism in these two types of FCs. METHODS: GSE28829, GSE43292, GSE68021, and GSE54666 were included to identify the differentially expressed genes (DEGs) associated with FCs derived from SMCs and macrophages. Gene Ontology biological process (GO-BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed by using the DAVID database. The co-regulated genes associated with the two origins of FCs were validated (GSE9874), and their expression in vulnerable atherosclerosis plaques (GSE120521 and GSE41571) was assessed. RESULTS: A total of 432 genes associated with FCs derived from SMCs (SMC-FCs) and 81 genes associated with FCs derived from macrophages (M-FCs) were identified, and they were mainly involved in lipid metabolism, inflammation, cell cycle/apoptosis. Furthermore, three co-regulated genes associated with FCs were identified: GLRX, RNF13, and ABCA1. These three common genes showed an increased tendency in unstable or ruptured plaques, although in some cases, no statistically significant difference was found. CONCLUSIONS: DEGs related to FCs derived from SMCs and macrophages have contributed to the understanding of the molecular mechanism underlying the formation of FCs and atherosclerosis. GLRX, RNF13, and ABCA1 might be potential targets for atherosclerosis treatment. PeerJ Inc. 2020-11-17 /pmc/articles/PMC7678445/ /pubmed/33240650 http://dx.doi.org/10.7717/peerj.10336 Text en ©2020 Zhang et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Bioinformatics
Zhang, Kai
Qin, Xianyu
Zhou, Xianwu
Zhou, Jianrong
Wen, Pengju
Chen, Shaoxian
Wu, Min
Wu, Yueheng
Zhuang, Jian
Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title_full Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title_fullStr Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title_full_unstemmed Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title_short Analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
title_sort analysis of genes and underlying mechanisms involved in foam cells formation and atherosclerosis development
topic Bioinformatics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7678445/
https://www.ncbi.nlm.nih.gov/pubmed/33240650
http://dx.doi.org/10.7717/peerj.10336
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