|Author||Soumyarani, V. S. ♦ Jayakumari, N.|
|Source||Sree Chitra Tirunal Institute for Medical Sciences & Technology|
|Publisher||Molecular and Cellular Biochemistry|
|Subject Domain (in DDC)||Technology ♦ Medicine & health|
|Subject Domain (in MeSH)||Immune System Phenomena ♦ Biological Sciences|
|Abstract||It has been proposed that high-density lipoprotein (HDL) loses its cardioprotective ability through oxidative modifications by reactive oxygen species (ROS) and promote atherogenesis. However, the pro-atherogenic pathways undergone by oxidized HDL remain poorly understood. Since monocytes play a crucial role in atherogenesis, this study was aimed to investigate the influence of both native and oxidized HDL (oxHDL) on monocytes-macrophages functions relevant to atherogenesis. HDL particles were isolated from human blood samples by ultracentrifugation and subjected to invitro oxidation with CuSO4. The extent of oxidation was quantitated by measurement of lipid peroxides. Human peripheral blood mononuclear cells were isolated and cultured under standard conditions. Cells were treated with native and oxHDL at varying concentrations for different time intervals and used for several analyses. Intracellular ROS production was assessed based on ROS-mediated DCFH fluorescence of the cells. The release of TNF-alpha and matrix metalloproteinases (MMPs) was quantitated using ELISA kit and gelatine zymography, respectively. Treatment of cells with oxidized HDL enhanced the production of ROS in a concentration-dependent way, while native HDL had no such effect. Further, the release of TNF-alpha, MMP-9, and MMP-2 was found to be remarkably higher in cells incubated with oxHDL than that of native HDL. Results demonstrate that oxidative modification of HDL induces pro-inflammatory response and oxidative stress in human monocytes-macrophages.|
|Education Level||UG and PG|
|Learning Resource Type||Article|
|Educational Framework||Medical Council of India (MCI)|
|Journal||MOLECULAR AND CELLULAR BIOCHEMISTRY|
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