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- Title
Dysfunction of endothelial progenitor cells in hyperlipidemic rats involves the increase of NADPH oxidase derived reactive oxygen species production.
- Authors
Li, Ting-Bo; Zhang, Jie-Jie; Liu, Bin; Luo, Xiu-Ju; Ma, Qi-Lin; Peng, Jun
- Abstract
NADPH oxidase (NOX) is a major source of reactive oxygen species (ROS) in the body and it plays a key role in mediation of oxidative injury in the cardiovascular system. The purposes of this study are to evaluate the status of NOX in endothelial progenitor cells (EPCs) of hyperlipidemic rats and to determine whether NOX-derived ROS promotes the dysfunction of EPCs. The rats were fed on a high-fat diet for 8 weeks to establish a hyperlipidemic rat model, which showed the increased plasma lipids and the impaired functions of circulating EPCs (including the reduced abilities in migration and adhesion) accompanied by an increase in NOX activity and ROS production. Next, EPCs were isolated from normal rats and they were treated with oxidized low-density lipoprotein (ox-LDL) (100 μg/mL) for 24 h to induce a dysfunctional model in vitro. In agreement with our findings in vivo, ox-LDL treatment increased the dysfunctions of EPCs concomitant with an increase in NOX activity and ROS production; these phenomena were reversed by the NOX inhibitor. Based on these observations, we conclude that NOX-derived ROS involved in the dysfunctions of circulating EPCs in hyperlipidemic rats and inhibition of NOX might provide a novel strategy to improve EPC functions in hyperlipidemia.
- Subjects
HYPERLIPIDEMIA; NADPH oxidase; REACTIVE oxygen species; PROGENITOR cells; ENDOTHELIAL cells; LIPOPROTEINS
- Publication
Canadian Journal of Physiology & Pharmacology, 2017, Vol 95, Issue 5, p474
- ISSN
0008-4212
- Publication type
Article
- DOI
10.1139/cjpp-2016-0142