2021年9月
Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914-5p suppression.
Biochemistry and biophysics reports
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- 巻
- 27
- 号
- 開始ページ
- 101046
- 終了ページ
- 101046
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.bbrep.2021.101046
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.
- リンク情報
- ID情報
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- DOI : 10.1016/j.bbrep.2021.101046
- PubMed ID : 34179516
- PubMed Central 記事ID : PMC8214032