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Ambient fine particulate matter induces endothelial progenitor cells apoptosis via reactive oxygen species formation
Author(s) -
Cui Yuqi,
Xie Xiaoyun,
Jia Fengpeng,
He Jianfeng,
Li Zhihong,
Fu Minghuan,
Hao Hong,
Liu Ying,
Liu Jason,
Cowan Peter,
Zhu Hua,
Sun Qinghua,
Liu Zhenguo
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.411.2
Subject(s) - reactive oxygen species , progenitor cell , superoxide dismutase , apoptosis , population , chemistry , glutathione peroxidase , oxidative stress , immunology , microbiology and biotechnology , andrology , stem cell , biology , biochemistry , medicine , environmental health
Background/Aims Bone marrow (BM)‐derived endothelial progenitor cells (EPCs) play a critical role in the angiogenesis. Some environmental insults, like fine particulate matter (PM) exposure, significantly inhibit EPCs‐mediated functions. However, the mechanisms remain largely unknown. The present research was to study the detrimental effects of PMon EPCs and explore the potential mechanisms. Methods PMwas intranasal‐distilled into male C57BL/6 mice for one month. Flow cytometry was used to measure the total number, apoptosis 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, PMwas 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. Funding sources: NIH R01 HL094650; AHA 12SDG12070174