Up-regulated miR-106b inhibits ox-LDL-induced endothelial cell apoptosis in atherosclerosis

Area of Science:

• Molecular Biology
• Cardiovascular Research
• Cell Biology

Background:

• Atherosclerosis (AS) involves endothelial cell apoptosis.
• MicroRNAs (miRNAs) play critical roles in cellular processes.
• The specific role of miR-106b in AS-related endothelial cell apoptosis requires elucidation.

Purpose of the Study:

• To investigate the molecular mechanism of microRNA (miR)-106b in the apoptosis of human aortic endothelial cells (HAECs) induced by oxidized-low-density lipoproteins (ox-LDL).
• To identify the target gene of miR-106b and its role in regulating endothelial cell apoptosis in AS.
• To explore the potential involvement of the PI3K/AKT signaling pathway.

Main Methods:

• Cell culture models using HAECs exposed to ox-LDL.
• Quantitative real-time PCR and Western blot to measure gene and protein expression.
• Apoptosis assays including TdT-mediated biotinylated nick end-labeling and flow cytometry.
• Luciferase reporter gene assay to confirm target gene interaction.

Main Results:

• MiR-106b expression was significantly downregulated in ox-LDL-treated HAECs.
• Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was identified as a direct target gene of miR-106b.
• Overexpression of miR-106b inhibited ox-LDL-induced HAEC apoptosis, an effect attenuated by PTEN overexpression.
• MiR-106b activation of the PI3K/AKT pathway was mediated by PTEN downregulation.

Conclusions:

• MiR-106b plays a protective role against endothelial cell apoptosis in atherosclerosis.
• The miR-106b/PTEN axis regulates endothelial cell apoptosis, potentially via the PI3K/AKT signaling pathway.
• Targeting miR-106b may represent a novel therapeutic strategy for atherosclerosis.