IMR Press / FBL / Volume 20 / Issue 6 / DOI: 10.2741/4351

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Oxidized low-density lipoprotein alters endothelial progenitor cell populations
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1 Dorothy M. Davis Heart and Lung Research Institute, Division of Cardiovascular Medicine, Department of Internal Medicine, Wexner Medical Center, The Ohio State University, Columbus, OH, USA
2 Burnett School of Biomedical Sciences, University of Central Florida College of Medicine, Orlando, FL, USA
3 Department of Medicine, University of Melbourne, and Immunology Research Centre, St. Vincent’s Hospital, Melbourne, Australia
4 Department of Cardiology, Shandong Provincial Hospital, Shandong University, Jinan, China
Academic Editor:Xiao-Feng Yang
Front. Biosci. (Landmark Ed) 2015, 20(6), 975–988; https://doi.org/10.2741/4351
Published: 1 June 2015
(This article belongs to the Special Issue Amylin in vasodilation, energy expenditure and inflammation)
Abstract

Oxidized low-density lipoprotein (ox-LDL) is critical to atherosclerosis in hyperlipidemia. Bone marrow (BM)-derived endothelial progenitor cells (EPCs) are important in preventing atherosclerosis, however these cells are significantly decreased in number in hyperlipidemia. This study aimed to determine whether ox-LDL and hyperlipidemia exert similar effects on EPC populations, and to investigate the involvement of reactive oxygen species (ROS). ROS production in BM and blood was significantly increased in male C57BL/6 mice treated with intravenous ox-LDL, and in hyperlipidemic LDL receptor knockout mice fed with a 4-month high-fat diet. ROS formation was effectively blocked by overexpression of antioxidant enzymes or N-acetylcysteine treatment. In both hyperlipidemic and ox-LDL-treated mice, the number of c-Kit+/CD31+ cells in BM and blood and of Sca-1+/Flk-1+ cells in blood significantly decreased, whereas the number of blood CD34+/Flk-1+ cells increased. In contrast, the number of blood CD34+/CD133+ cells increased in ox-LDL-treated mice but decreased in hyperlipidemic mice. Only the changes in CD34+/Flk-1+ cell number were prevented by inhibiting ROS production. These data suggested that ox-LDL produced significant changes in BM and blood EPC populations, largely similar to chronic hyperlipidemia, via predominantly ROS-independent mechanism(s).

Keywords
ox-LDL
hyperlipidemia
NAC
ROS
EPC
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