Triglyceride-rich lipoprotein lipolysis increases aggregation of endothelial cell membrane microdomains and produces reactive oxygen species

摘要: Triglyceride-rich lipoprotein (TGRL) lipolysis may provide a proinflammatory stimulus to endothelium. Detergent-resistant plasma membrane microdomains (lipid rafts) have number of functions in endothelial cell inflammation. The mechanisms TGRL lipolysis-induced injury were investigated by examining lipid rafts and production reactive oxygen species (ROS). Lipid raft human aortic cells visualized confocal microscopy with fluorescein isothiocyanate-labeled cholera toxin B as marker. Incubation Atto565-labeled raft-labeled showed that colocalized the rafts, caused clustering aggregation colocalization remnant particles on aggregated rafts. Furthermore, translocation low-density receptor-related protein, nitric oxide synthase, caveolin-1 from regions nonraft 3 h after treatment lipolysis. significantly increased ROS cells, both NADPH oxidase cytochrome P-450 inhibitors reduced ROS. Our studies suggest alteration morphology composition could contribute lipolysis-mediated injury.