Evaluation of fine particulate matter on vascular endothelial function in vivo and in vitro.

Ambient fine particulate matter (PM) and high-fat diet (HFD) are linked to the development of atherosclerosis. However, there is still unknown about the PM-induced atherosclerosis formation on vascular endothelial injury after co-exposed to PM and HFD. Thus, the aim of this study was to evaluate the effects of PM on atherogenesis in C57BL/6 mice and endothelial cells, as well as the co-exposure effect of PM and HFD. In vivo study, C57BL/6 mice exposed to PM and fed with standard chow diet (STD) or HFD for 1 month. PM could increase vascular stiffness accessed by Doppler ultrasound, and more serious in co-exposure group. PM impaired vascular endothelial layer integrity, exfoliated endothelial cells, and inflammatory cells infiltration through H&E staining. PM reduced the expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) in vessel. Moreover, PM could induce systemic inflammation detected by Mouse Inflammation Array. In vitro study, PM triggered markedly mitochondrial damage by transmission electron microscope (TEM) and flow cytometer. Inflammatory cytokines were significantly increased in PM-exposed group. The cell viability and migration of endothelial cells were significantly suppressed. In addition, PM remarkably declined the expression of vascular endothelial growth factor receptor 2 (VEGFR2) and increased the expression of somatostatin (SST) and its receptor. In conclusion, co-exposure of PM and HFD might induce systemic inflammation and endothelial dysfunction in normal mice. Moreover, PM could reduce vascular endothelial repair capacity through inhibiting the proliferation and migration of endothelial cells.