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Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression

Atherosclerosis is a chronic inflammatory disease and the underlying cause of most cardiovascular diseases. Interleukin (IL)-1β facilitates early atherogenic lesion formation by increasing monocyte adhesion to endothelial cells via upregulation of adhesion molecules, including intercellular adhesion...

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Detalles Bibliográficos
Autores principales: Kihara, Toshie, Toriuchi, Kohki, Aoki, Hiromasa, Kakita, Hiroki, Yamada, Yasumasa, Aoyama, Mineyoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8214032/
https://www.ncbi.nlm.nih.gov/pubmed/34179516
http://dx.doi.org/10.1016/j.bbrep.2021.101046
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author Kihara, Toshie
Toriuchi, Kohki
Aoki, Hiromasa
Kakita, Hiroki
Yamada, Yasumasa
Aoyama, Mineyoshi
author_facet Kihara, Toshie
Toriuchi, Kohki
Aoki, Hiromasa
Kakita, Hiroki
Yamada, Yasumasa
Aoyama, Mineyoshi
author_sort Kihara, Toshie
collection PubMed
description Atherosclerosis is a chronic inflammatory disease and the underlying cause of most cardiovascular diseases. Interleukin (IL)-1β facilitates early atherogenic lesion formation by increasing monocyte adhesion to endothelial cells via upregulation of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1). MicroRNAs (miRNAs) have been shown to be associated with inflammatory conditions in the vascular system. The expression of circulating miR-1914–5p is reportedly downregulated in patients with cardiovascular diseases. However, the role of miR-1914–5p downregulation in IL-1β–induced endothelial cell dysfunction and the effect of miR-1914–5p on lesion formation remain unclear. Therefore, we investigated whether miR-1914–5p is associated with monocyte adhesion in human endothelial cells. IL-1β decreased miR-1914–5p expression in EA.hy926 cells. In addition, miR-1914–5p depletion enhanced ICAM-1 expression and monocyte adhesion in EA.hy926 cells. Moreover, miR-1914–5p mimic suppressed monocyte adhesion and ICAM-1 expression induced by IL-1β in endothelial cells. These results suggest that suppression of miR-1914–5p expression by IL-1β may be an important regulator in mediating monocyte adhesion in endothelial cells. Further investigation of miR-1914–5p may lead to the development of novel therapeutic strategies for atherosclerosis.
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spelling pubmed-82140322021-06-25 Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression Kihara, Toshie Toriuchi, Kohki Aoki, Hiromasa Kakita, Hiroki Yamada, Yasumasa Aoyama, Mineyoshi Biochem Biophys Rep Research Article Atherosclerosis is a chronic inflammatory disease and the underlying cause of most cardiovascular diseases. Interleukin (IL)-1β facilitates early atherogenic lesion formation by increasing monocyte adhesion to endothelial cells via upregulation of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1). MicroRNAs (miRNAs) have been shown to be associated with inflammatory conditions in the vascular system. The expression of circulating miR-1914–5p is reportedly downregulated in patients with cardiovascular diseases. However, the role of miR-1914–5p downregulation in IL-1β–induced endothelial cell dysfunction and the effect of miR-1914–5p on lesion formation remain unclear. Therefore, we investigated whether miR-1914–5p is associated with monocyte adhesion in human endothelial cells. IL-1β decreased miR-1914–5p expression in EA.hy926 cells. In addition, miR-1914–5p depletion enhanced ICAM-1 expression and monocyte adhesion in EA.hy926 cells. Moreover, miR-1914–5p mimic suppressed monocyte adhesion and ICAM-1 expression induced by IL-1β in endothelial cells. These results suggest that suppression of miR-1914–5p expression by IL-1β may be an important regulator in mediating monocyte adhesion in endothelial cells. Further investigation of miR-1914–5p may lead to the development of novel therapeutic strategies for atherosclerosis. Elsevier 2021-06-12 /pmc/articles/PMC8214032/ /pubmed/34179516 http://dx.doi.org/10.1016/j.bbrep.2021.101046 Text en © 2021 The Authors. Published by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Kihara, Toshie
Toriuchi, Kohki
Aoki, Hiromasa
Kakita, Hiroki
Yamada, Yasumasa
Aoyama, Mineyoshi
Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title_full Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title_fullStr Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title_full_unstemmed Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title_short Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914–5p suppression
title_sort interleukin-1β enhances cell adhesion in human endothelial cells via microrna-1914–5p suppression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8214032/
https://www.ncbi.nlm.nih.gov/pubmed/34179516
http://dx.doi.org/10.1016/j.bbrep.2021.101046
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