We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Ox-LDL Induces Dysfunction of Endothelial Progenitor Cells via Activation of NF-κB.
- Authors
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; Ma, Jun; Liao, Lian-ming; Tang, Ji-fei
- 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.
- Subjects
ATHEROSCLEROSIS risk factors; HYPERLIPIDEMIA; REACTIVE oxygen species; BIOLOGICAL assay; CELL culture; CELL physiology; ENDOTHELIUM; IMMUNOHISTOCHEMISTRY; INFLAMMATION; LOW density lipoproteins; OXIDIZING agents; PROTEINS; RESEARCH funding; ALBUMINS; FLUORESCENT dyes; DIAGNOSIS
- Publication
BioMed Research International, 2015, Vol 2015, p1
- ISSN
2314-6133
- Publication type
Article
- DOI
10.1155/2015/175291