As an anti-inflammatory cytokine, interleukin-37 (IL-37) provides certain protective effects against inflammatory and autoimmune diseases. Recent reports indicate that IL-37 is expressed in foam cells of atherosclerotic plaques in both the coronary and carotid arteries of humans, suggesting the possible involvement of IL-37 in the pathogenesis and progression of atherosclerosis. Current evidence supports the protective role that IL-37 plays against atherosclerosis via the regulation of different subtypes of macrophage.
The aim of this study was to identify potential markers of atherosclerosis development in familial hypercholesterolemia (FH) patients. GSE13985 microarray data, generated using blood samples from 5 FH patients and 5 matched controls, was downloaded from the Gene Expression Omnibus. Differentially expressed genes (DEGs) between FH and controls were identified and a protein-protein interaction (PPI) network was constructed. Module and hub proteins were screened in this network.
Our study aimed to investigate the effects of interleukin-4 (IL-4) on macrophage polarization, as well as its role in the development of atherosclerosis. Human peripheral blood mononuclear cells (PBMCs) were isolated and randomly divided into 3 groups: control group, ox-LDL group, and ox-LDL + IL-4 groups. The expression of M1/M2 macrophage surface markers such as TNF-α, CD68, and CD206 were analyzed by western blot. Cell viability was determined using the MTT assay. Measurement of CD86/CD206 expression ratio (M1/M2 ratio) was performed via flow cytometry.