Adiponectin Suppresses oxLDL-Induced Vascular Cell Inflammation, Proliferation, and Migration, thus Attenuating Atherosclerosis

Abstract

Backgrounds: Atherosclerosis is a chronic and progressive vascular disease. Adiponectin, a hormone produced by adipose tissue, has been implicated in the development of atherosclerosis. Therefore, this study aims to explore the biological functions of Adiponectin in vascular cells and its impact on the progression of atherosclerosis. Methods: Initially, atherosclerosis-related cell models were established in human coronary artery endothelial cells (HCAEC), human mononuclear cell line (THP-1), and vascular smooth muscle cells (VSMC) by stimulating them with Oxidized Low-Density Lipoprotein (oxLDL). The impact of adiponectin on the proliferation and migration capabilities of oxLDL-stimulated HCAEC, THP-1, and VSMC cells was assessed using the Cell Counting Kit-8 (CCK-8) method and the Transwell assay. The influence of adiponectin on the expression levels of inflammatory factors as well as the levels of Protein Kinase B (AKT) and phosphorylated AKT was determined in oxLDL-stimulated HCAEC, THP-1, and VSMC cells employing Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) and western blot analysis. Results: Adiponectin inhibited the proliferation and migration capabilities of oxLDL-stimulated HCAEC, THP-1, and VSMC cells (p < 0.01, and p < 0.001). Additionally, adiponectin reduced inflammation by modulating the mRNA expression of inflammatory factors in HCAEC, THP-1, and VSMC cells (p < 0.05, p < 0.01, and p < 0.001). Furthermore, Adiponectin decreased the phosphorylation levels of AKT in oxLDL-induced HCAEC, THP-1, and VSMC cells (p < 0.01, and p < 0.001). Conclusions: This study suggests that adiponectin may play a role in attenuating atherosclerosis by inhibiting AKT phosphorylation, impeding the migration and proliferation of vascular cells, and reducing inflammation.