Glycolaldehyde induces synergistic effects on vascular inflammation in TNF-α-stimulated vascular smooth muscle cells

Atherosclerosis is a chronic inflammatory disease that contributes to disease progression is associated with the expression of adhesion molecules in vascular smooth muscle cells (VSMCs). Glycolaldehyde (GA) has been shown to impair cellular function in various disorders, including diabetes, and renal diseases. This study investigated the effect of GA on the expression of adhesion molecules in the mouse VSMC line, MOVAS-1. Co-incubation of VSMCs with GA (25-50 mu M) dose-dependently increased the protein and mRNA level of Vcam-1 and ICAM-1. Additionally, GA upregulated intracellular ROS production and phosphorylation of MAPK and NK-kappa B. GA also elevated TNF-alpha-induced PI3K-AKT activation. Furthermore, GA enhanced TNF-alpha-activated I kappa B alpha kinase activation, subsequent I kappa B alpha degradation, and nuclear translocation of NF-kappa B. These findings suggest that GA stumulated VSMC adhesive capacity and the induction of VCAM-1 and ICAM-1 in VSMCs through inhibition of MAPK and NF-kappa B signaling pathways, providing insights into the effect of GA to induce inflammation within atherosclerotic lesions.

Automated summary

Glycolaldehyde (GA) stimulates adhesive capacity and induces the expression of VCAM-1 and ICAM-1 in VSMCs through inhibition of MAPK and NF-kappa B signaling pathways, providing new insights into GA-induced inflammation within atherosclerotic lesions.