Ox-LDL Induces Dysfunction of Endothelial Progenitor Cells via Activation of NF-κB

Abstract EN

Dyslipidemia increases the risks for atherosclerosis in part by impairing endothelial integrity.

Endothelial progenitor cells (EPCs) are thought to contribute to endothelial recovery after arterial injury.

Oxidized low-density lipoprotein (ox-LDL) can induce EPC dysfunction, but the underlying mechanism is not well understood.

Human EPCs were cultured in endothelial growth medium supplemented with VEGF (10 ng/mL) and bFGF (10 ng/mL).

The cells were treated with ox-LDL (50 µg/mL).

EPC proliferation was assayed by using CCK8 kits.

Expression and translocation of nuclear factor-kabba B (NF-κB) were evaluated.

The level of reactive oxygen species (ROS) in cells was measured using H2DCF-DA as a fluorescence probe.

The activity of NADPH oxidase activity was determined by colorimetric assay.

Ox-LDL significantly decreased the proliferation, migration, and adhesion capacity of EPCs, while significantly increased ROS production and NADPH oxidase expression.

Ox-LDL induced NF-κB P65 mRNA expression and translocation in EPCs.

Thus ox-LDL can induce EPC dysfunction at least by increasing expression and translocation of NF-κB P65 and NADPH oxidase activity, which represents a new mechanism of lipidemia-induced vascular injury.