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Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients
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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Association of Internal Medicine
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840593/ https://www.ncbi.nlm.nih.gov/pubmed/28899085 http://dx.doi.org/10.3904/kjim.2016.140 |
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author | Li, Ting-Bo Zhang, Yin-Zhuang Liu, Wei-Qi Zhang, Jie-Jie Peng, Jun Luo, Xiu-Ju Ma, Qi-Lin |
author_facet | Li, Ting-Bo Zhang, Yin-Zhuang Liu, Wei-Qi Zhang, Jie-Jie Peng, Jun Luo, Xiu-Ju Ma, Qi-Lin |
author_sort | Li, Ting-Bo |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5840593 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | The Korean Association of Internal Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-58405932018-03-08 Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients Li, Ting-Bo Zhang, Yin-Zhuang Liu, Wei-Qi Zhang, Jie-Jie Peng, Jun Luo, Xiu-Ju Ma, Qi-Lin Korean J Intern Med Original Article 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. The Korean Association of Internal Medicine 2018-03 2017-09-13 /pmc/articles/PMC5840593/ /pubmed/28899085 http://dx.doi.org/10.3904/kjim.2016.140 Text en Copyright © 2018 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Li, Ting-Bo Zhang, Yin-Zhuang Liu, Wei-Qi Zhang, Jie-Jie Peng, Jun Luo, Xiu-Ju Ma, Qi-Lin Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title | Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title_full | Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title_fullStr | Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title_full_unstemmed | Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title_short | Correlation between NADPH oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
title_sort | correlation between nadph oxidase-mediated oxidative stress and dysfunction of endothelial progenitor cell in hyperlipidemic patients |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840593/ https://www.ncbi.nlm.nih.gov/pubmed/28899085 http://dx.doi.org/10.3904/kjim.2016.140 |
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