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

• Published in: PloS one Vol. 17; no. 7; p. e0270249
• Main Authors: Lee, Hee-Weon, Gu, Min Ji, Yoo, Guijae, Choi, In-Wook, Lee, Sang-Hoon, Kim, Yoonsook, Ha, Sang Keun
• Format: Journal Article
• Language: English
• Published: San Francisco Public Library of Science 01.07.2022; Public Library of Science (PLoS)
• Subjects: 1-Phosphatidylinositol 3-kinase; Adhesion; Age; AKT protein; Antibodies; Arteriosclerosis; Atherosclerosis; Biology and Life Sciences; Blood vessels; Cell adhesion molecules; Cell growth; Cytokines; Diabetes; Diabetes mellitus; Disease; Free radicals; Glycolaldehyde; Inflammation; Inflammatory diseases; Intercellular adhesion molecule 1; Kinases; MAP kinase; Medicine and Health Sciences; Microscopy; mRNA; Muscles; NF-κB protein; Nuclear transport; Oxidative stress; Phosphorylation; Proteins; Research and Analysis Methods; Smooth muscle; Synergistic effect; Translocation; Tumor necrosis factor-α; Vascular cell adhesion molecule 1; St Louis Missouri; United States > US
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0270249

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 μM) 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-κB. GA also elevated TNF-α-induced PI3K-AKT activation. Furthermore, GA enhanced TNF-α-activated IκBα kinase activation, subsequent IκBα degradation, and nuclear translocation of NF-κB. 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-κB signaling pathways, providing insights into the effect of GA to induce inflammation within atherosclerotic lesions.