RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability
Abstract Carotid artery atherosclerosis is a risk factor to develop cerebrovascular disease. Atheroma plaque can become instable and provoke a cerebrovascular event or else remain stable as asymptomatic type. The exact mechanism involved in plaque destabilization is not known but includes among othe...
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oai:doaj.org-article:337e64c41ab24272b95be14cb051acf22021-12-02T15:05:53ZRNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability10.1038/s41598-017-03687-92045-2322https://doaj.org/article/337e64c41ab24272b95be14cb051acf22017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-03687-9https://doaj.org/toc/2045-2322Abstract Carotid artery atherosclerosis is a risk factor to develop cerebrovascular disease. Atheroma plaque can become instable and provoke a cerebrovascular event or else remain stable as asymptomatic type. The exact mechanism involved in plaque destabilization is not known but includes among other events smooth muscle cell (SMC) differentiation. The goal of this study was to perform thorough analysis of gene expression differences in SMCs isolated from carotid symptomatic versus asymptomatic plaques. Comparative transcriptomics analysis of SMCs based on RNAseq technology identified 67 significant differentially expressed genes and 143 significant differentially expressed isoforms in symptomatic SMCs compared with asymptomatic. 37 of top-scoring genes were further validated by digital PCR. Enrichment and network analysis shows that the gene expression pattern of SMCs from stable asymptomatic plaques is suggestive for an osteogenic phenotype, while that of SMCs from unstable symptomatic plaque correlates with a senescence-like phenotype. Osteogenic-like phenotype SMCs may positively affect carotid atheroma plaque through participation in plaque stabilization via bone formation processes. On the other hand, plaques containing senescence-like phenotype SMCs may be more prone to rupture. Our results substantiate an important role of SMCs in carotid atheroma plaque disruption.Iraide AllozaHaize GoikuriaJuan Luis IdroJuan Carlos TriviñoJosé María Fernández VelascoElena ElizagarayMaría García-BarcinaGenoveva Montoya-MurilloEsther SarasolaReyes Vega ManriqueMaria del Mar FreijoKoen VandenbroeckNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017) |
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Medicine R Science Q Iraide Alloza Haize Goikuria Juan Luis Idro Juan Carlos Triviño José María Fernández Velasco Elena Elizagaray María García-Barcina Genoveva Montoya-Murillo Esther Sarasola Reyes Vega Manrique Maria del Mar Freijo Koen Vandenbroeck RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
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Abstract Carotid artery atherosclerosis is a risk factor to develop cerebrovascular disease. Atheroma plaque can become instable and provoke a cerebrovascular event or else remain stable as asymptomatic type. The exact mechanism involved in plaque destabilization is not known but includes among other events smooth muscle cell (SMC) differentiation. The goal of this study was to perform thorough analysis of gene expression differences in SMCs isolated from carotid symptomatic versus asymptomatic plaques. Comparative transcriptomics analysis of SMCs based on RNAseq technology identified 67 significant differentially expressed genes and 143 significant differentially expressed isoforms in symptomatic SMCs compared with asymptomatic. 37 of top-scoring genes were further validated by digital PCR. Enrichment and network analysis shows that the gene expression pattern of SMCs from stable asymptomatic plaques is suggestive for an osteogenic phenotype, while that of SMCs from unstable symptomatic plaque correlates with a senescence-like phenotype. Osteogenic-like phenotype SMCs may positively affect carotid atheroma plaque through participation in plaque stabilization via bone formation processes. On the other hand, plaques containing senescence-like phenotype SMCs may be more prone to rupture. Our results substantiate an important role of SMCs in carotid atheroma plaque disruption. |
format |
article |
author |
Iraide Alloza Haize Goikuria Juan Luis Idro Juan Carlos Triviño José María Fernández Velasco Elena Elizagaray María García-Barcina Genoveva Montoya-Murillo Esther Sarasola Reyes Vega Manrique Maria del Mar Freijo Koen Vandenbroeck |
author_facet |
Iraide Alloza Haize Goikuria Juan Luis Idro Juan Carlos Triviño José María Fernández Velasco Elena Elizagaray María García-Barcina Genoveva Montoya-Murillo Esther Sarasola Reyes Vega Manrique Maria del Mar Freijo Koen Vandenbroeck |
author_sort |
Iraide Alloza |
title |
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
title_short |
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
title_full |
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
title_fullStr |
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
title_full_unstemmed |
RNAseq based transcriptomics study of SMCs from carotid atherosclerotic plaque: BMP2 and IDs proteins are crucial regulators of plaque stability |
title_sort |
rnaseq based transcriptomics study of smcs from carotid atherosclerotic plaque: bmp2 and ids proteins are crucial regulators of plaque stability |
publisher |
Nature Portfolio |
publishDate |
2017 |
url |
https://doaj.org/article/337e64c41ab24272b95be14cb051acf2 |
work_keys_str_mv |
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