miR-291b-3p mediated ROS-induced endothelial cell dysfunction by targeting HUR

Area of Science:

• Cardiovascular Biology
• Molecular Medicine
• Cellular Biology

Background:

• Endothelial dysfunction is an early indicator of atherosclerosis.
• MicroRNA (miR)-291b-3p is known to regulate lipid and glucose metabolism in the liver.
• The role of miR-291b-3p in oxidative stress-induced endothelial dysfunction requires further investigation.

Purpose of the Study:

• To investigate the role of miR-291b-3p in hydrogen peroxide (H2O2)-induced endothelial dysfunction.
• To identify the molecular targets of miR-291b-3p in endothelial cells.

Main Methods:

• EOMA mouse endothelial cells were treated with H2O2.
• Apoptosis was assessed using terminal deoxynucleotidyl-transferase-mediated dUTP nick end labelling (TUNEL) staining.
• mRNA and protein levels of miR-291b-3p, ICAM-1, VCAM-1, phosphorylated ERK, Bcl-2-associated X protein (Bax), Bcl-2, and Hu antigen R (HuR) were analyzed using quantitative PCR and western blotting.
• miR-291b-3p mimics and inhibitors were used to modulate its expression.

Main Results:

• H2O2 treatment induced apoptosis and increased miR-291b-3p, ICAM-1, and VCAM-1 mRNA levels in EOMA cells.
• Overexpression of miR-291b-3p promoted apoptosis and dysfunction in EOMA cells.
• Downregulation of miR-291b-3p rescued H2O2-induced endothelial dysfunction.
• HuR was identified as a direct target of miR-291b-3p.
• Overexpression of HuR reversed the endothelial dysfunction caused by miR-291b-3p mimics.

Conclusions:

• miR-291b-3p plays a critical role in mediating H2O2-induced endothelial dysfunction.
• miR-291b-3p may exert its effects by targeting HuR in endothelial cells.
• These findings offer novel insights into the molecular mechanisms underlying endothelial dysfunction in response to oxidative stress.