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Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity

Cigarette smoking is a risk factor for the development of peripheral artery disease (PAD), although the proatherosclerotic mediators of cigarette smoking are not entirely known. We explored whether circulating microRNAs (miRNAs) are dysregulated in cigarette smokers and associated with the presence...

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Autores principales: Pereira-da-Silva, Tiago, Napoleão, Patrícia, Costa, Marina C., Gabriel, André F., Selas, Mafalda, Silva, Filipa, Enguita, Francisco J., Ferreira, Rui Cruz, Carmo, Miguel Mota
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926909/
https://www.ncbi.nlm.nih.gov/pubmed/33671744
http://dx.doi.org/10.3390/jcm10040890
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author Pereira-da-Silva, Tiago
Napoleão, Patrícia
Costa, Marina C.
Gabriel, André F.
Selas, Mafalda
Silva, Filipa
Enguita, Francisco J.
Ferreira, Rui Cruz
Carmo, Miguel Mota
author_facet Pereira-da-Silva, Tiago
Napoleão, Patrícia
Costa, Marina C.
Gabriel, André F.
Selas, Mafalda
Silva, Filipa
Enguita, Francisco J.
Ferreira, Rui Cruz
Carmo, Miguel Mota
author_sort Pereira-da-Silva, Tiago
collection PubMed
description Cigarette smoking is a risk factor for the development of peripheral artery disease (PAD), although the proatherosclerotic mediators of cigarette smoking are not entirely known. We explored whether circulating microRNAs (miRNAs) are dysregulated in cigarette smokers and associated with the presence of PAD. Ninety-four participants were recruited, including 58 individuals without and 36 with PAD, 51 never smokers, 28 prior smokers, and 15 active smokers. The relative expression of six circulating miRNAs with distinct biological roles (miR-21, miR-27b, miR-29a, miR-126, miR-146, and miR-218) was assessed. Cigarette smoking was associated with the presence of PAD in multivariate analysis. Active smokers, but not prior smokers, presented miR-27b downregulation and higher leukocyte, neutrophil, and lymphocyte counts; miR-27b expression levels were independently associated with active smoking. Considering the metabolic and/or inflammatory abnormalities induced by cigarette smoking, miR-27b was independently associated with the presence of PAD and downregulated in patients with more extensive PAD. In conclusion, the atheroprotective miR-27b was downregulated in active smokers, but not in prior smokers, and miR-27b expression was independently associated with the presence of PAD. These unreported data suggest that the proatherogenic properties of cigarette smoking are mediated by a downregulation of miR-27b, which may be attenuated by smoking cessation.
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spelling pubmed-79269092021-03-04 Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity Pereira-da-Silva, Tiago Napoleão, Patrícia Costa, Marina C. Gabriel, André F. Selas, Mafalda Silva, Filipa Enguita, Francisco J. Ferreira, Rui Cruz Carmo, Miguel Mota J Clin Med Article Cigarette smoking is a risk factor for the development of peripheral artery disease (PAD), although the proatherosclerotic mediators of cigarette smoking are not entirely known. We explored whether circulating microRNAs (miRNAs) are dysregulated in cigarette smokers and associated with the presence of PAD. Ninety-four participants were recruited, including 58 individuals without and 36 with PAD, 51 never smokers, 28 prior smokers, and 15 active smokers. The relative expression of six circulating miRNAs with distinct biological roles (miR-21, miR-27b, miR-29a, miR-126, miR-146, and miR-218) was assessed. Cigarette smoking was associated with the presence of PAD in multivariate analysis. Active smokers, but not prior smokers, presented miR-27b downregulation and higher leukocyte, neutrophil, and lymphocyte counts; miR-27b expression levels were independently associated with active smoking. Considering the metabolic and/or inflammatory abnormalities induced by cigarette smoking, miR-27b was independently associated with the presence of PAD and downregulated in patients with more extensive PAD. In conclusion, the atheroprotective miR-27b was downregulated in active smokers, but not in prior smokers, and miR-27b expression was independently associated with the presence of PAD. These unreported data suggest that the proatherogenic properties of cigarette smoking are mediated by a downregulation of miR-27b, which may be attenuated by smoking cessation. MDPI 2021-02-22 /pmc/articles/PMC7926909/ /pubmed/33671744 http://dx.doi.org/10.3390/jcm10040890 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Pereira-da-Silva, Tiago
Napoleão, Patrícia
Costa, Marina C.
Gabriel, André F.
Selas, Mafalda
Silva, Filipa
Enguita, Francisco J.
Ferreira, Rui Cruz
Carmo, Miguel Mota
Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title_full Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title_fullStr Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title_full_unstemmed Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title_short Cigarette Smoking, miR-27b Downregulation, and Peripheral Artery Disease: Insights into the Mechanisms of Smoking Toxicity
title_sort cigarette smoking, mir-27b downregulation, and peripheral artery disease: insights into the mechanisms of smoking toxicity
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7926909/
https://www.ncbi.nlm.nih.gov/pubmed/33671744
http://dx.doi.org/10.3390/jcm10040890
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