Title: Ambient fine particulate matter induces apoptosis of endothelial progenitor cells through reactive oxygen species formation.
Authors: Cui, Yuqi; Xie, Xiaoyun; Jia, Fengpeng; He, Jianfeng; Li, Zhihong; Fu, Minghuan; Hao, Hong; Liu, Ying; Liu, Jason Z; Cowan, Peter J; Zhu, Hua; Sun, Qinghua; Liu, Zhenguo
Published In Cell Physiol Biochem, (2015)
Abstract: Bone marrow (BM)-derived endothelial progenitor cells (EPCs) play a critical role in angiogenesis and vascular repair. Some environmental insults, like fine particulate matter (PM) exposure, significantly impair cardiovascular functions. However, the mechanisms for PM-induced adverse effects on cardiovascular system remain largely unknown. The present research was to study the detrimental effects of PM on EPCs and explore the potential mechanisms.PM was intranasal-distilled into male C57BL/6 mice for one month. Flow cytometry was used to measure the number of EPCs, apoptosis level of circulating EPCs and intracellular reactive oxygen species (ROS) formation. Serum TNF-α and IL-1β were measured using ELISA. To determine the role of PM-induced ROS in EPC apoptosis, PM was co-administrated with the antioxidant N-acetylcysteine (NAC) in wild type mice or used in a triple transgenic mouse line (TG) with overexpression of antioxidant enzyme network (AON) composed of superoxide dismutase (SOD)1, SOD3, and glutathione peroxidase (Gpx-1) with decreased in vivo ROS production.PM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-α and IL-1β levels, which could be effectively reversed by either NAC treatment or overexpression of AON.PM exposure significantly decreased circulating EPCs population due to increased apoptosis via ROS formation in mice.
PubMed ID: 25591776
MeSH Terms: Acetylcysteine/pharmacology; Animals; Apoptosis/drug effects*; Bone Marrow Cells/cytology; Cells, Cultured; Endothelial Progenitor Cells/cytology; Endothelial Progenitor Cells/drug effects; Endothelial Progenitor Cells/metabolism; Enzyme-Linked Immunosorbent Assay; Glutathione Peroxidase/genetics; Glutathione Peroxidase/metabolism; Interleukin-1beta/blood; Lung/metabolism; Lung/pathology; Male; Mice; Mice, Inbred C57BL; Particulate Matter/toxicity*; Reactive Oxygen Species/metabolism*; Superoxide Dismutase-1; Superoxide Dismutase/genetics; Superoxide Dismutase/metabolism; Tumor Necrosis Factor-alpha/blood