Ambient Fine Particulate Matter Induces Apoptosis of Endothelial Progenitor Cells Through Reactive Oxygen Species Formation

作者：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^*

来源：Cellular Physiology and Biochemistry, 2015, 35(1): 353-363.

DOI：10.1159/000369701

• PM
• Endothelial progenitor cells
• ROS
• Apoptosis

Background/Aims: 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. Methods: 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- alpha and IL-1 beta 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. Results: PM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-alpha and IL-1 beta levels, which could be effectively reversed by either NAC treatment or overexpression of AON. Conclusion: PM exposure significantly decreased circulating EPCs population due to increased apoptosis via ROS formation in mice.

• 出版日期2015