CD5L Secreted by Macrophage on Atherosclerosis Progression Based on Lipid Metabolism Induced Inflammatory Damage

Abstract

To explore the molecular mechanism of exosomal protein CD5L secreted by macrophage to promote the progression of atherosclerosis. Twenty cases of patients with atherosclerosis (AS) and 20 cases of healthy subjects were collected. Morphological properties of exosomes were identified by transmission electron microscopy, and the marker proteins CD63 and CD81 of exosomes were measured by Western blot. The secretion of inflammatory factors in the blood supernatant were analyzed by ELISA. Atherosclerosis cell models were established by transwell and separated into three groups: first group was treated with exosome inhibitor (GW4869), second group was injected with CD5L protein and third group was model control. Morphological properties of exosomes were identified by transmission electron microscopy, and the marker proteins CD63 and CD81 of exosomes were measured by Western blot. The levels of TNF-α, IL-1β, IL-6, IL-13, IL-17A, IL-31 in the cells were analyzed by ELISA. Analysis of the expression and distribution of IL-17RA in vascular smooth muscle cells by immunofluorescence. The proteins of CD63, CD81, CD5L were high expressed in AS group compared to healthy subject group. Cell test results showed that protein levels of CD63, CD81, CD5L in AS group were much higher than that in normal group. Immunofluorescence showed that the expression level of IL-17RA in cell membrane was the highest in the AS model group, and the expression of IL-17RA was decreased in GW4869 group and CD5L group. Expression of inflammatory factors in AS was much higher than that in GW4869 group and CD5L group. The exosomal protein CD5L secreted by macrophage promotes the development of atherosclerosis based on lipid metabolism-induced inflammatory damage of vascular smooth muscle cells.