Ox-LDL Induces Dysfunction of Endothelial Progenitor Cells via Activation of NF-κB

Content Provider	Semantic Scholar
Author	Ji, Kang-Ting Qian, Lu Nan, Jin-Liang Xue, Yang-Jing Zhang, Su-Qin Wang, Guo-Qiang Yin, Ri-Peng Zhu, Yong-Jin Wang, Lu-Ping Liao, Lian-Ming Tang, Ji-Fei
Copyright Year	2015
Abstract	Dyslipidemia increases the risks for atherosclerosis in part by impairing endothelial integrity. Endothelial progenitor cells (EPCs) are thought to contribute to endothelial recovery after arterial injury. Oxidized low-density lipoprotein (ox-LDL) can induce EPC dysfunction, but the underlying mechanism is not well understood. Human EPCs were cultured in endothelial growth medium supplemented with VEGF (10 ng/mL) and bFGF (10 ng/mL). The cells were treated with ox-LDL (50 µg/mL). EPC proliferation was assayed by using CCK8 kits. Expression and translocation of nuclear factor-kabba B (NF-κB) were evaluated. The level of reactive oxygen species (ROS) in cells was measured using H2DCF-DA as a fluorescence probe. The activity of NADPH oxidase activity was determined by colorimetric assay. Ox-LDL significantly decreased the proliferation, migration, and adhesion capacity of EPCs, while significantly increased ROS production and NADPH oxidase expression. Ox-LDL induced NF-κB P65 mRNA expression and translocation in EPCs. Thus ox-LDL can induce EPC dysfunction at least by increasing expression and translocation of NF-κB P65 and NADPH oxidase activity, which represents a new mechanism of lipidemia-induced vascular injury.
File Format	PDF HTM / HTML
DOI	10.1155/2015/175291
PubMed reference number	25821786
Journal	Medline
Volume Number	2015
Alternate Webpage(s)	http://downloads.hindawi.com/journals/bmri/2015/175291.pdf
Alternate Webpage(s)	https://doi.org/10.1155/2015%2F175291
Journal	BioMed research international
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article