The Investigation Of Proliferation And Migration Of Vascular Smooth Muscle Cells Induced By Oxidized High-density Lipoprotein

AIM:High-density lipoprotein (HDL) is the major atheroprotectiveparticle in plasma, and can be oxidized during systemic inflammation, includingatherosclerosis. Oxidized HDL (ox-HDL) may lose its cardioprotective propertiesand develop proinflammatory and proatherogenic phenotype. Proliferation andmigration of vascular smooth muscle cells (VSMCs) play a crucial role inatherogenesis, however, the influence of ox-HDL on VSMCs proliferation andmigration remains poorly understood.Methods:HDL was isolated from human blood samples byultracentrifugation and subjected to oxidation with CuSO4in vitro. Rat aorticVSMCs were isolated and cultured under standard conditions. VSMCs were treatedwith native HDL (N-HDL) or ox-HDL at varying concentrations for different timeintervals and used for several analyses. Cell proliferation was assayed with CCK-8kits. Cell migration was determined with a transwell chamber and a scratch-woundassay. Intracellular reactive oxygen species (ROS) production was assessed based onROS-mediated DCF fluorescence.Results:Our results showed that N-HDL had no effects on theproliferation and migration in VSMCs,however, ox-HDL significantly promotedVSMCs proliferation and migration in a dose-dependent manner. In addition, wealso observed that ox-HDL remarkably enhanced ROS generation in aconcentration-dependent manner in VSMCs, while N-HDL did not have this effect.N-Acetylcysteine (NAC), a ROS scavenger, could efficiently inhibit ROS productiontriggered by ox-HDL, and subsequently blocked the proliferative and promigrativeeffects of ox-HDL in VSMCs.Conclusions:Thus our results elucidated that oxidative modification ofHDL induces the proliferation and migration of VSMCs via promoting theproduction of ROS,which could be closely related to its atherogenic roles.