Exposure to Ambient Air Fine Particulate Matter Prevents VEGF-Induced Mobilization of Endothelial Progenitor Cells from the Bone Marrow

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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Abstract 409: Ambient Fine Particulate Matter Impairs Endothelial Progenitor Cells Through Card9-mediated Innate Immune Response

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.38.suppl_1.409 ◽

2018 ◽

Vol 38 (Suppl_1) ◽

Author(s):

Yuqi Cui ◽

Xuanyou Liu ◽

Zhiheng Chen ◽

Huifang Xu ◽

Hong Hao ◽

...

Keyword(s):

Immune Response ◽

Particulate Matter ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Innate Immune Response ◽

Fine Particulate Matter ◽

Innate Immune ◽

Endothelial Progenitor ◽

Fine Particulate

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

International Journal of Molecular Sciences ◽

10.3390/ijms22137200 ◽

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.

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

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.35.suppl_1.565 ◽

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.

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

Cellular Physiology and Biochemistry ◽

10.1159/000369701 ◽

2015 ◽

Vol 35 (1) ◽

pp. 353-363 ◽

Cited By ~ 38

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.

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