1. Ambient fine particulate matter induces apoptosis of endothelial progenitor cells through reactive oxygen species formation.
- Author
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Cui Y, Xie X, Jia F, He J, Li Z, Fu M, Hao H, Liu Y, Liu JZ, Cowan PJ, Zhu H, Sun Q, and Liu Z
- Subjects
- Acetylcysteine pharmacology, Animals, 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, Superoxide Dismutase genetics, Superoxide Dismutase metabolism, Superoxide Dismutase-1, Tumor Necrosis Factor-alpha blood, Apoptosis drug effects, Particulate Matter toxicity, Reactive Oxygen Species metabolism
- Abstract
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., (© 2015 S. Karger AG, Basel.)
- Published
- 2015
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