miR-150-5p affects AS plaque with ASMC proliferation and migration by STAT1

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• MicroRNA Therapeutics

Background:

• Atherosclerosis (AS) is a chronic inflammatory disease characterized by lipid plaque buildup in arteries.
• MicroRNAs play critical roles in regulating cellular processes relevant to AS pathogenesis.
• The specific role of miR-150-5p in AS progression requires further elucidation.

Purpose of the Study:

• To investigate the role of miR-150-5p in atherosclerosis.
• To determine the therapeutic potential of modulating miR-150-5p in AS.
• To elucidate the molecular mechanism involving STAT1.

Main Methods:

• Atherosclerosis model in Apo E^-/- mice.
• In vitro studies using oxidized low-density lipoprotein (ox-LDL)-stimulated human aortic smooth muscle cells (ASMCs).
• Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blot, Oil red O staining, Masson staining, and dual-luciferase reporter assay.

Main Results:

• miR-150-5p expression was decreased in AS mice and ox-LDL-treated ASMCs, while STAT1 expression was increased.
• miR-150-5p inhibition exacerbated AS pathology, whereas its upregulation alleviated plaque formation and collagen accumulation.
• miR-150-5p directly targeted STAT1, inhibiting ASMC viability, migration, and cell cycle progression.
• Overexpression of STAT1 counteracted the protective effects of miR-150-5p mimic.

Conclusions:

• miR-150-5p acts as a protective factor in atherosclerosis.
• Modulating miR-150-5p may offer a therapeutic strategy for AS.
• The miR-150-5p/STAT1 axis regulates ASMC proliferation and migration, contributing to plaque stabilization.