Abstract 565: Ambient Fine Particulate Matter Decreases Endothelial Progenitor Cells Through Reactive Oxygen Species-mediated Apoptosis

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Yuqi Cui ◽  
Xiaoyun Xie ◽  
Jason Z Liu ◽  
Fengpeng Jia ◽  
Jianfeng He ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Particulate Matter ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fine Particulate Matter ◽  
Ros Production ◽  
Oxygen Species ◽  
Fine Particulate ◽  
Tnf Α ◽  
Ros Formation

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.

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

2015 ◽  
Vol 35 (1) ◽  
pp. 353-363 ◽  
Author(s):  
Yuqi Cui ◽  
Xiaoyun Xie ◽  
Fengpeng Jia ◽  
Jianfeng He ◽  
Zhihong Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Particulate Matter ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fine Particulate Matter ◽  
Ros Production ◽  
Oxygen Species ◽  
Fine Particulate ◽  
Tnf Α ◽  
Ros Formation

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.

scholarly journals Circulating Endothelial Progenitor Cells Are Preserved in Female Mice Exposed to Ambient Fine Particulate Matter Independent of Estrogen

2021 ◽  
Vol 22 (13) ◽  
pp. 7200
Author(s):  
Xuanyou Liu ◽  
Yichao Xiao ◽  
Qingyi Zhu ◽  
Yuqi Cui ◽  
Hong Hao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Particulate Matter ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fine Particulate Matter ◽  
Serum Levels ◽  
Ros Production ◽  
Male Mice ◽  
Female Mice ◽  
Fine Particulate

Males have a higher risk for cardiovascular diseases (CVDs) than females. Ambient fine particulate matter (PM) exposure increases CVD risk with increased reactive oxygen species (ROS) production and oxidative stress. Endothelial progenitor cells (EPCs) are important to vascular structure and function and can contribute to the development of CVDs. The aims of the present study were to determine if sex differences exist in the effect of PM exposure on circulating EPCs in mice and, if so, whether oxidative stress plays a role. Male and female C57BL/6 mice (8–10 weeks old) were exposed to PM or a vehicle control for six weeks. ELISA analysis showed that PM exposure substantially increased the serum levels of IL-6 and IL-1β in both males and females, but the concentrations were significantly higher in males. PM exposure only increased the serum levels of TNF-α in males. Flow cytometry analysis demonstrated that ROS production was significantly increased by PM treatment in males but not in females. Similarly, the level of circulating EPCs (CD34+/CD133+ and Sca-1+/Flk-1+) was significantly decreased by PM treatment in males but not in females. Antioxidants N-acetylcysteine (NAC) effectively prevented PM exposure-induced ROS and inflammatory cytokine production and restored circulating EPC levels in male mice. In sharp contrast, circulating EPC levels remained unchanged in female mice with PM exposure, an effect that was not altered by ovariectomy. In conclusion, PM exposure selectively decreased the circulating EPC population in male mice via increased oxidative stress without a significant impact on circulating EPCs in females independent of estrogen.

Reactive oxygen species (ROS) activity of fine particulate matter health impacts in Addis Ababa, Ethiopia

2021 ◽  
pp. 101149
Author(s):  
Piyaporn Sricharoenvech ◽  
Alexandra Lai ◽  
Worku Tefera ◽  
Abera Kumie ◽  
Kiros Berhane ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Particulate Matter ◽  
Addis Ababa ◽  
Fine Particulate Matter ◽  
Reactive Oxygen ◽  
Health Impacts ◽  
Oxygen Species ◽  
Fine Particulate

scholarly journals Dysfunction of endothelial progenitor cells in hyperlipidemic rats involves the increase of NADPH oxidase derived reactive oxygen species production

2017 ◽  
Vol 95 (5) ◽  
pp. 474-480 ◽  
Author(s):  
Ting-Bo Li ◽  
Jie-Jie Zhang ◽  
Bin Liu ◽  
Xiu-Ju Luo ◽  
Qi-Lin Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Plasma Lipids ◽  
Reactive Oxygen ◽  
The Body ◽  
Ros Production ◽  
Oxygen Species ◽  
Endothelial Progenitor

NADPH oxidase (NOX) is a major source of reactive oxygen species (ROS) in the body and it plays a key role in mediation of oxidative injury in the cardiovascular system. The purposes of this study are to evaluate the status of NOX in endothelial progenitor cells (EPCs) of hyperlipidemic rats and to determine whether NOX-derived ROS promotes the dysfunction of EPCs. The rats were fed on a high-fat diet for 8 weeks to establish a hyperlipidemic rat model, which showed the increased plasma lipids and the impaired functions of circulating EPCs (including the reduced abilities in migration and adhesion) accompanied by an increase in NOX activity and ROS production. Next, EPCs were isolated from normal rats and they were treated with oxidized low-density lipoprotein (ox-LDL) (100 μg/mL) for 24 h to induce a dysfunctional model in vitro. In agreement with our findings in vivo, ox-LDL treatment increased the dysfunctions of EPCs concomitant with an increase in NOX activity and ROS production; these phenomena were reversed by the NOX inhibitor. Based on these observations, we conclude that NOX-derived ROS involved in the dysfunctions of circulating EPCs in hyperlipidemic rats and inhibition of NOX might provide a novel strategy to improve EPC functions in hyperlipidemia.

scholarly journals Exposure to Fine Particulate Matter Air Pollution Alters mRNA and miRNA Expression in Bone Marrow-Derived Endothelial Progenitor Cells from Mice

Genes ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 1058
Author(s):  
Xiaohong Li ◽  
Petra Haberzettl ◽  
Daniel J. Conklin ◽  
Aruni Bhatnagar ◽  
Eric C. Rouchka ◽  
...  
Keyword(s):  
Gene Expression ◽  
Air Pollution ◽  
Particulate Matter ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mirna Expression ◽  
Fine Particulate Matter ◽  
Cell Movement ◽  
Endothelial Progenitor ◽  
Fine Particulate

Exposure to fine particulate matter (PM2.5) air pollution is associated with quantitative deficits of circulating endothelial progenitor cells (EPCs) in humans. Related exposures of mice to concentrated ambient PM2.5 (CAP) likewise reduces levels of circulating EPCs and induces defects in their proliferation and angiogenic potential as well. These changes in EPC number or function are predictive of larger cardiovascular dysfunction. To identify global, PM2.5-dependent mRNA and miRNA expression changes that may contribute to these defects, we performed a transcriptomic analysis of cells isolated from exposed mice. Compared with control samples, we identified 122 upregulated genes and 44 downregulated genes in EPCs derived from CAP-exposed animals. Functions most impacted by these gene expression changes included regulation of cell movement, cell and tissue development, and cellular assembly and organization. With respect to miRNA changes, we found that 55 were upregulated while 53 were downregulated in EPCs from CAP-exposed mice. The top functions impacted by these miRNA changes included cell movement, cell death and survival, cellular development, and cell growth and proliferation. A subset of these mRNA and miRNA changes were confirmed by qRT-PCR, including some reciprocal relationships. These results suggest that PM2.5-induced changes in gene expression may contribute to EPC dysfunction and that such changes may contribute to the adverse cardiovascular outcomes of air pollution exposure.

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