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Updated: Dec 6, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-188-3p Inhibits Vascular Smooth Muscle Cell Proliferation and Migration by Targeting Fibroblast Growth Factor 1
Shaohua Mi1, Pengfei Wang2, Lejun Lin3
1Department of Cardiology, Yantai Yuhuangding Hospital, Qingdao University, Yantai, Shandong, China (mainland).
Abstract:
BACKGROUND As one of the crucial causes leading to cardiovascular disease, atherosclerosis (AS) develops in association with the dysfunction of vascular smooth muscle cells (VSMCs). However, the associated mechanism of the proliferation and migration in VSMCs requires further elucidation. MATERIAL AND METHODS Human VSMCs and ApoE-knockout (ApoE-/-) mice were used to establish AS cell and animal models, respectively. Expression levels of miR-188-3p and fibroblast growth factor 1 (FGF1) mRNA were detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Western blot was used to assess FGF1 protein expression. The proliferation, migration, and apoptosis of the cells were determined using MTT, BrdU, and Transwell assays, as well as flow cytometry analysis. The interaction between miR-188-3p and FGF1 was validated using dual-luciferase reporter gene assay, qRT-PCR, and Western blot analysis. RESULTS MiR-188-3p was found to be significantly decreased in the serum of AS patients and ApoE-/- mice as well as VSMCs of ApoE-/- mice and human VSMCs treated with oxidized low-density lipoprotein. MiR-188-3p repressed the proliferation and migration of VSMCs but promoted apoptosis of VSMCs. The binding site between miR-188-3p and 3' untranslated region (3'-UTR) of FGF1 was identified, and FGF1 was verified as a target gene of miR-188-3p. Restoration of FGF1 reversed the effects of miR-188-3p on VSMCs. CONCLUSIONS MiR-188-3p suppresses the proliferation and migration of VSMCs and induces their apoptosis through targeting FGF1.
Insights
MicroRNA-188-3p, a crucial molecule in atherosclerosis, inhibits vascular smooth muscle cell proliferation and migration while promoting apoptosis. This microRNA targets fibroblast growth factor 1 (FGF1), offering potential therapeutic insights for cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Atherosclerosis (AS) is a major cause of cardiovascular disease, linked to vascular smooth muscle cell (VSMC) dysfunction.
- The precise mechanisms regulating VSMC proliferation and migration in AS require further investigation.
Purpose of the Study:
- To elucidate the role of miR-188-3p in regulating VSMC behavior.
- To identify the molecular targets and pathways involved in miR-188-3p's function in AS.
Main Methods:
- Established AS cell and mouse models using human VSMCs and ApoE-knockout mice.
- Quantified miR-188-3p and fibroblast growth factor 1 (FGF1) expression via qRT-PCR and Western blot.
- Assessed VSMC proliferation, migration, and apoptosis using MTT, BrdU, Transwell assays, and flow cytometry.
- Validated miR-188-3p and FGF1 interaction using dual-luciferase reporter assays.
Main Results:
- miR-188-3p levels were significantly decreased in AS patients, ApoE-/- mice, and VSMCs exposed to oxidized LDL.
- miR-188-3p suppressed VSMC proliferation and migration while promoting apoptosis.
- FGF1 was identified as a direct target gene of miR-188-3p.
- Restoring FGF1 expression reversed the effects of miR-188-3p on VSMCs.
Conclusions:
- miR-188-3p acts as a suppressor of VSMC proliferation and migration.
- miR-188-3p induces VSMC apoptosis by targeting FGF1.
- This microRNA-target interaction presents a novel mechanism in atherosclerosis development.
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