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

Ambient fine particulate matter (PM_2.5) and high-fat diet (HFD) are linked to the development of atherosclerosis. However, there is still unknown about the PM_2.5-induced atherosclerosis formation on vascular endothelial injury after co-exposed to PM_2.5 and HFD. Thus, the aim of this study was to evaluate the effects of PM_2.5 on atherogenesis in C57BL/6 mice and endothelial cells, as well as the co-exposure effect of PM_2.5 and HFD. In vivo study, C57BL/6 mice exposed to PM_2.5 and fed with standard chow diet (STD) or HFD for 1 month. PM_2.5 could increase vascular stiffness accessed by Doppler ultrasound, and more serious in co-exposure group. PM_2.5 impaired vascular endothelial layer integrity, exfoliated endothelial cells, and inflammatory cells infiltration through H&E staining. PM_2.5 reduced the expression of platelet/endothelial cell adhesion molecule-1 (PECAM-1) in vessel. Moreover, PM_2.5 could induce systemic inflammation detected by Mouse Inflammation Array. In vitro study, PM_2.5 triggered markedly mitochondrial damage by transmission electron microscope (TEM) and flow cytometer. Inflammatory cytokines were significantly increased in PM_2.5-exposed group. The cell viability and migration of endothelial cells were significantly suppressed. In addition, PM_2.5 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_2.5 and HFD might induce systemic inflammation and endothelial dysfunction in normal mice. Moreover, PM_2.5 could reduce vascular endothelial repair capacity through inhibiting the proliferation and migration of endothelial cells.