ArticleBiochemistry and biophysics reports2021
Interleukin-1β enhances cell adhesion in human endothelial cells via microRNA-1914-5p suppression.
Article in Biochemistry and biophysics reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
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- Foam cells: tracing the diverse cellular origins and their linked signaling pathways.Journal of translational medicine · 2025Review
- Exploring the predictive potentials of IL-1β and TNFR1 in atherogenic risk in prediabetes.Scientific reports · 2025Article
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- Herpes Simplex Virus ICP27 Protein Inhibits AIM 2-Dependent Inflammasome Influencing Pro-Inflammatory Cytokines Release in Human Pigment Epithelial Cells (hTert-RPE 1).International journal of molecular sciences · 2024Article
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- Role of human dural fibroblasts in the angiogenic responses of human endothelial cells: An in vitro dural model and the application of lab-on-a-chip for EDAS.Bioengineering & translational medicine · 2023Article
- Review
- Monocyte-Derived miRNA-1914-5p Attenuates IL-1β-Induced Monocyte Adhesion and Transmigration.International journal of molecular sciences · 2023Article
- Inhibition of IRAK1 Is an Effective Therapy for Autoimmune Hypophysitis in Mice.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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