Abstract
Bone marrow (BM)‐derived endothelial progenitor cells (EPCs) make significant contribution to the function and integrity of vasculature. The number of EPCs is significantly decreased in hyperlipidemic patients. Oxidized low‐density lipoprotein (ox‐LDL) is a major component of hyperlipidemia and contributing to atherosclerosis. The present study was to determine if ox‐LDL could change EPC populations and the role of reactive oxygen species (ROS). EPC numbers and ROS formation in BM and blood were determined in male C57BL/6 mice treated with ox‐LDL intraveneously. Flow cytometry analysis and EPR measurement showed that the ROS production in both BM and blood was significantly increased in ox‐LDL‐treated mice that was effectively blocked with concomitant overexpression of copper/zinc superoxide dismutase (SOD1), extracellular SOD3, and glutathione peroxidase or N‐acetylcysteine treatment. Ox‐LDL treatment produced complex changes in EPC populations in BM and blood. In ox‐LDL‐treated mice, the c‐Kit+/CD31+ cell number was significantly decreased in BM and blood, and the Sca‐1+/Flk‐1+ cell number was significantly decreased in blood but not in BM. Ox‐LDL decreased the cell population of c‐Kit+/CD31+ in BM and blood, and the Sca‐1+/Flk‐1+ cell number in blood with a mechanism predominantly independent of ROS production in vivo.
Published Version
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