Abstract
The vascular endothelium is the center of events leading to the development of inflammatory lesions. The activation of endothelial cells is of significance in acute as well as chronic inflammatory states such as septic shock and atherosclerosis, respectively. Receptor for advanced glycation end products (RAGE) plays a role in immune reaction to recognize specific molecular patterns as pathogen recognition receptors. However, the function of RAGE in LPS‐induced inflammation is unclear. In this study, we investigated whether RAGE is enrolled in lipopolysaccharide (LPS)‐induced cell activation in human umbilical vein endothelial cells (HUVECs) using a combination of western blotting, confocal microscopy, and functional assays. We found that LPS can directly increase the expression of RAGE in a time‐ and concentration‐ dependent manner. And anti‐RAGE antibody inhibited LPS‐mediated barrier high‐permeability and apoptosis of HUVECs. Furthermore, LPS‐induced NF‐κB activation and IκBα degradation was also significantly attenuated by anti‐RAGE antibody. Given these results, RAGE plays an important role in LPS‐induced inflammation and could be a candidate as a therapeutic target for various systemic inflammatory diseases.Grant Funding Source: AHA
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