Cargando…
Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation
Carotid atherosclerosis is a chronic inflammatory disease of the arterial wall. The present study aimed to identify changes in the gene expression and regulatory factors for atherosclerotic plaques of carotid atherosclerosis from an early to an advanced stage. The original data were downloaded from...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214333/ https://www.ncbi.nlm.nih.gov/pubmed/25318463 http://dx.doi.org/10.3892/ijmm.2014.1960 |
_version_ | 1782341941934948352 |
---|---|
author | LIN, MIN ZHAO, LIN ZHAO, WENLONG WENG, JING |
author_facet | LIN, MIN ZHAO, LIN ZHAO, WENLONG WENG, JING |
author_sort | LIN, MIN |
collection | PubMed |
description | Carotid atherosclerosis is a chronic inflammatory disease of the arterial wall. The present study aimed to identify changes in the gene expression and regulatory factors for atherosclerotic plaques of carotid atherosclerosis from an early to an advanced stage. The original data were downloaded from the NCBI GEO database under accession no. GSE28829. Differentially expressed genes (DEGs) were detected by the Robust Multiarray Average (RMA). The enriched Gene Ontology (GO) terms and pathways for DEGs using DAVID were subsequently identified. The transcriptional and microRNA (miRNA) regulatory network were constructed for the DEGs. Cis-regulatory signals were also investigated. More genes were activated in the advanced stage compared with the early stage. IGHG1 and SPP1 were upregulated, while MYBL1 and PLD were downregulated. The upregulated genes in the advanced stage were involved in atherosclerosis-related GO terms such as immune, vascular and cell movement homeostasis. The DEGs were significantly enriched in cell adhesion molecules (CAMs) and the focal adhesion pathway. MMP9 and CFL2 played key roles in the transcriptional regulatory network. Moreover, miR-328 was identified as one of the hubs in the miRNA regulatory network. The results may therefore be used to determine the mechanism involved in carotid atherosclerosis. |
format | Online Article Text |
id | pubmed-4214333 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-42143332014-10-30 Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation LIN, MIN ZHAO, LIN ZHAO, WENLONG WENG, JING Int J Mol Med Articles Carotid atherosclerosis is a chronic inflammatory disease of the arterial wall. The present study aimed to identify changes in the gene expression and regulatory factors for atherosclerotic plaques of carotid atherosclerosis from an early to an advanced stage. The original data were downloaded from the NCBI GEO database under accession no. GSE28829. Differentially expressed genes (DEGs) were detected by the Robust Multiarray Average (RMA). The enriched Gene Ontology (GO) terms and pathways for DEGs using DAVID were subsequently identified. The transcriptional and microRNA (miRNA) regulatory network were constructed for the DEGs. Cis-regulatory signals were also investigated. More genes were activated in the advanced stage compared with the early stage. IGHG1 and SPP1 were upregulated, while MYBL1 and PLD were downregulated. The upregulated genes in the advanced stage were involved in atherosclerosis-related GO terms such as immune, vascular and cell movement homeostasis. The DEGs were significantly enriched in cell adhesion molecules (CAMs) and the focal adhesion pathway. MMP9 and CFL2 played key roles in the transcriptional regulatory network. Moreover, miR-328 was identified as one of the hubs in the miRNA regulatory network. The results may therefore be used to determine the mechanism involved in carotid atherosclerosis. D.A. Spandidos 2014-12 2014-10-09 /pmc/articles/PMC4214333/ /pubmed/25318463 http://dx.doi.org/10.3892/ijmm.2014.1960 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles LIN, MIN ZHAO, LIN ZHAO, WENLONG WENG, JING Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title | Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title_full | Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title_fullStr | Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title_full_unstemmed | Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title_short | Dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
title_sort | dissecting the mechanism of carotid atherosclerosis from the perspective of regulation |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214333/ https://www.ncbi.nlm.nih.gov/pubmed/25318463 http://dx.doi.org/10.3892/ijmm.2014.1960 |
work_keys_str_mv | AT linmin dissectingthemechanismofcarotidatherosclerosisfromtheperspectiveofregulation AT zhaolin dissectingthemechanismofcarotidatherosclerosisfromtheperspectiveofregulation AT zhaowenlong dissectingthemechanismofcarotidatherosclerosisfromtheperspectiveofregulation AT wengjing dissectingthemechanismofcarotidatherosclerosisfromtheperspectiveofregulation |