MiR-483-5p downregulation alleviates ox-LDL induced endothelial cell injury in atherosclerosis

Area of Science:

• Biomedical research
• Molecular biology
• Cardiovascular science

Background:

• Atherosclerosis (AS) is linked to abnormal microRNA-483-5p (miR-483-5p) expression.
• The role of miR-483-5p in vascular endothelial cell injury requires further investigation.
• Mechanisms involving autophagy in this process need elucidation.

Purpose of the Study:

• To explore the role of miR-483-5p in endothelial cell injury.
• To investigate the underlying mechanisms, particularly those related to autophagy.
• To understand the therapeutic potential of modulating miR-483-5p in atherosclerosis.

Main Methods:

• Human umbilical vein endothelial cells (HUVECs) were treated with ox-LDL to induce injury.
• miR-483-5p levels were modulated via cell transfection.
• Cell viability, apoptosis, and mRNA levels (including inflammatory markers) were assessed using qRT-PCR.
• Autophagic flux was monitored, and autophagy inhibition was employed using 3-MA.

Main Results:

• Ox-LDL treatment impaired autophagic flux and upregulated miR-483-5p in HUVECs.
• Downregulation of miR-483-5p improved cell viability and reduced apoptosis.
• miR-483-5p downregulation decreased pro-inflammatory markers (IL-1β, IL-6, ICAM-1, VCAM-1).
• Autophagy inhibition reversed the protective effects of miR-483-5p downregulation.
• TIMP2 was identified as a target gene of miR-483-5p and was downregulated.

Conclusions:

• Downregulation of miR-483-5p alleviates ox-LDL-induced endothelial injury.
• This protective effect is mediated through the activation of autophagy.
• The mechanism may involve the regulation of TIMP2 by miR-483-5p.