Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients.
- Author:
Ting Bo LI
1
;
Yin Zhuang ZHANG
;
Wei Qi LIU
;
Jie Jie ZHANG
;
Jun PENG
;
Xiu Ju LUO
;
Qi Lin MA
Author Information
- Publication Type:Original Article
- Keywords: NADPH oxidase; Hyperlipidemias; Endothelial progenitor cells; Reactive oxygen species; Oxidized low-density lipoprotein
- MeSH: Adenine; Cardiovascular System; Endothelial Progenitor Cells*; Humans; Hyperlipidemias; NADP*; NADPH Oxidase; Oxidative Stress*; Oxidoreductases; Plasma; Reactive Oxygen Species; Statistics as Topic; Volunteers
- From:The Korean Journal of Internal Medicine 2018;33(2):313-322
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND/AIMS: NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (NOX)-mediated oxidative stress plays a key role in promotion of oxidative injury in the cardiovascular system. The aim of this study is to evaluate the status of NOX in endothelial progenitor cells (EPCs) of hyperlipidemic patients and to assess the correlation between NOX activity and the functions EPCs. METHODS: A total of 30 hyperlipidemic patients were enrolled for this study and 30 age-matched volunteers with normal level of plasma lipids served as controls. After the circulating EPCs were isolated, the EPC functions (migration, adhesion and tube formation) were evaluated and the status of NOX (expression and activity) was examined. RESULTS: Compared to the controls, hyperlipidemic patients showed an increase in plasma lipids and a reduction in EPC functions including the attenuated abilities in adhesion, migration and tube formation, concomitant with an increase in NOX expression (NOX2 and NOX4), NOX activity, and reactive oxygen species production. The data analysis showed negative correlations between NOX activity and EPC functions. CONCLUSIONS: There is a positive correlation between the NOX-mediated oxidative stress and the dysfunctions of circulating EPCs in hyperlipidemic patients, and suppression of NOX might offer a novel strategy to improve EPCs functions in hyperlipidemia.
