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MicroRNA expression profile of human advanced coronary atherosclerotic plaques
MicroRNA (miR) is reported to be involved in vascular inflammation and may represent a novel class of diagnostic biomarkers in cardiovascular disease. We aimed to identify the miR expression profile in human advanced coronary atherosclerotic plaques (CAP) and to connect this expression to the proces...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959940/ https://www.ncbi.nlm.nih.gov/pubmed/29777114 http://dx.doi.org/10.1038/s41598-018-25690-4 |
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author | Parahuleva, Mariana S. Lipps, Christoph Parviz, Behnoush Hölschermann, Hans Schieffer, Bernhard Schulz, Rainer Euler, Gerhild |
author_facet | Parahuleva, Mariana S. Lipps, Christoph Parviz, Behnoush Hölschermann, Hans Schieffer, Bernhard Schulz, Rainer Euler, Gerhild |
author_sort | Parahuleva, Mariana S. |
collection | PubMed |
description | MicroRNA (miR) is reported to be involved in vascular inflammation and may represent a novel class of diagnostic biomarkers in cardiovascular disease. We aimed to identify the miR expression profile in human advanced coronary atherosclerotic plaques (CAP) and to connect this expression to the processes in atherosclerosis. Microarray techniques and TaqMan polymerase chain reaction were used to analyse the global expression of 352 miRs in CAP obtained during ACS MULTI-LINK study. 11 miRs were selected on the basis of their implication in atherosclerosis, endothelial activation, and inflammation. 6 miRs were found to be differently expressed in CAP when compared to non-atherosclerotic internal mammary arteries (IMA, p < 0.05). The expression of miR-21, -92a, and -99a was verified and found to be significantly up-regulated in CAP versus IMA (p < 0.001). We also performed bioinformatic analysis and found several potential target genes of miR-92a and -99a as well as several pathways with impact on atherosclerosis which could be differently expressed due to this miRNA profile. The most up-regulated miRs are involved in processes known to be connected to atherosclerosis. Interfering with the miR expression in the artery wall is a potential way to affect atherosclerotic plaque and cardiovascular disease development. |
format | Online Article Text |
id | pubmed-5959940 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-59599402018-05-24 MicroRNA expression profile of human advanced coronary atherosclerotic plaques Parahuleva, Mariana S. Lipps, Christoph Parviz, Behnoush Hölschermann, Hans Schieffer, Bernhard Schulz, Rainer Euler, Gerhild Sci Rep Article MicroRNA (miR) is reported to be involved in vascular inflammation and may represent a novel class of diagnostic biomarkers in cardiovascular disease. We aimed to identify the miR expression profile in human advanced coronary atherosclerotic plaques (CAP) and to connect this expression to the processes in atherosclerosis. Microarray techniques and TaqMan polymerase chain reaction were used to analyse the global expression of 352 miRs in CAP obtained during ACS MULTI-LINK study. 11 miRs were selected on the basis of their implication in atherosclerosis, endothelial activation, and inflammation. 6 miRs were found to be differently expressed in CAP when compared to non-atherosclerotic internal mammary arteries (IMA, p < 0.05). The expression of miR-21, -92a, and -99a was verified and found to be significantly up-regulated in CAP versus IMA (p < 0.001). We also performed bioinformatic analysis and found several potential target genes of miR-92a and -99a as well as several pathways with impact on atherosclerosis which could be differently expressed due to this miRNA profile. The most up-regulated miRs are involved in processes known to be connected to atherosclerosis. Interfering with the miR expression in the artery wall is a potential way to affect atherosclerotic plaque and cardiovascular disease development. Nature Publishing Group UK 2018-05-18 /pmc/articles/PMC5959940/ /pubmed/29777114 http://dx.doi.org/10.1038/s41598-018-25690-4 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Parahuleva, Mariana S. Lipps, Christoph Parviz, Behnoush Hölschermann, Hans Schieffer, Bernhard Schulz, Rainer Euler, Gerhild MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title | MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title_full | MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title_fullStr | MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title_full_unstemmed | MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title_short | MicroRNA expression profile of human advanced coronary atherosclerotic plaques |
title_sort | microrna expression profile of human advanced coronary atherosclerotic plaques |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959940/ https://www.ncbi.nlm.nih.gov/pubmed/29777114 http://dx.doi.org/10.1038/s41598-018-25690-4 |
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