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Updated: Apr 30, 2026
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-152 reduces human umbilical vein endothelial cell proliferation and migration by targeting ADAM17
Yang Wu1, Aixue Huang2, Tao Li3
1General Hospital of Chinese People's Liberation Army, Beijing 100853, PR China.
Abstract:
As a cleavage enzyme of precursor TNF-α, the high expression level of ADAM17 in endothelial cells is an important factor in atherosclerosis. In this study, we demonstrate that ADAM17 is the target of miR-152. We found that miR-152 could reduce TNF precursor cleavage and inhibit cell proliferation and migration by targeting ADAM17 in human umbilical vein endothelial cells (HUVECs). Furthermore, the expression pattern of miR-152 and corresponding target ADAM17 was opposite in HUVECs under hypoxic conditions. The levels of circulating miR-152 in AS patient sera were lower than those detected in the sera of normal individuals. Our results indicate that miR-152 may be involved in the development of human atherosclerosis and could be used as diagnostic biomarker or therapeutic target in atherosclerosis.
Insights
MicroRNA-152 (miR-152) targets ADAM17, reducing its role in endothelial cells and potentially inhibiting atherosclerosis development. Lower miR-152 levels in atherosclerosis patients suggest its diagnostic and therapeutic potential.
Area of Science:
- Biomedical research
- Molecular biology
- Cardiovascular disease
Background:
- ADAM17, a TNF-α precursor enzyme, is highly expressed in endothelial cells and implicated in atherosclerosis.
- Understanding the regulation of ADAM17 is crucial for developing atherosclerosis treatments.
Purpose of the Study:
- To investigate the regulatory relationship between miR-152 and ADAM17 in human umbilical vein endothelial cells (HUVECs).
- To explore the potential role of miR-152 as a biomarker and therapeutic target in atherosclerosis.
Main Methods:
- Investigated the targeting of ADAM17 by miR-152 in HUVECs.
- Analyzed the expression patterns of miR-152 and ADAM17 under hypoxic conditions.
- Compared circulating miR-152 levels in atherosclerosis (AS) patients and normal individuals.
Main Results:
- miR-152 was confirmed as a target of ADAM17, reducing TNF precursor cleavage.
- miR-152 inhibited proliferation and migration of HUVECs by targeting ADAM17.
- Opposite expression patterns of miR-152 and ADAM17 were observed in HUVECs under hypoxia.
- Circulating miR-152 levels were significantly lower in AS patients compared to controls.
Conclusions:
- miR-152 plays a role in regulating ADAM17 activity in endothelial cells.
- miR-152 may be involved in the pathogenesis of human atherosclerosis.
- miR-152 shows potential as a diagnostic biomarker and therapeutic target for atherosclerosis.
