Abstract 565: Ambient Fine Particulate Matter Decreases Endothelial Progenitor Cells Through Reactive Oxygen Species-mediated 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- 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.
Results: 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.
Conclusion: PM exposure significantly decreased circulating EPCs population due to increased apoptosis via ROS formation in mice.
Author Disclosures: Y. Cui: None. X. Xie: None. J.Z. Liu: None. F. Jia: None. J. He: None. H. Hao: None. Y. Liu: None. P.J. Cowan: None. H. Zhu: None. Q. Sun: None. Z. Liu: None.
- © 2015 by American Heart Association, Inc.