Increased expression of CD74 in atherosclerosis associated with inflammatory responses of endothelial cells and macrophages

Abstract

Abstract Background To clarify the relationship between CD74 and atherosclerosis (AS) and the mechanisms in oxidized LDL (ox-LDL)-induced endothelial cell and macrophage injury. Methods Datasets obtained from the Gene Expression Omnibus database are integrated. Differentially expressed genes (DEGs) were obtained using R software. Weighted gene co-expression network analysis (WGCNA) was performed to screen the target genes. The endothelial cell injury model and macrophage foaming model were established using ox-LDL, and CD74 expression was detected by Quantitative reverse transcription PCR (RT-qPCR) and Western blot (WB). Then, after silencing CD74, cell viability and ROS production were measured, and WB detected the expression of p-p38 MAPK and NF-κB. Results 268 DEGs were associated with AS, of which CD74 was upregulated. The turquoise module containing CD74 in WGCNA was positively associated with AS. In the endothelial cell injury model and macrophage foaming model, cell viability was significantly decreased, and CD74, ROS production, NF-κB, and p-p38MAPK expression were increased (P < 0.05). After silencing CD74, ROS production, NF-κB, and p-p38MAPK expression were decreased, and cell viability increased compared to the model group (P < 0.05). Conclusions CD74 is upregulated in endothelial cell injury and macrophage foaming models and is involved in AS progression via the NF-κB and MAPK signaling pathways.