Search for: [Abstract = "No increase in the expression of any of the analyzed genes was detected in endothelial cells exposed to PM2.5 collected near a busy road at concentration of 15 μg\/cm2. In contrast, the organic fraction obtained from the PM2.5 up\-regulated genes involved in repair of damaged endothelial cells\: fibronectin 1 \(FN1\) receptor 2 vascular endothelial growth factor \(VEGFR\-2\), von Willebrand factor, and metalloproteinase 2 \(MMP\-2\). These findings were suggestive of a low\-grade cell injury, as 4 hours after dosing mainly genes responsible for vascular endothelium repair were detected. A similar response was observed in case of ZnO NPs at a concentration of 5 μg\/cm2, which up\-regulated FN1, cell adhesion molecule ICAM\-1, ADAM17 glycoprotein, which stimulated the release of L\-selectin and TNFAPI3 protein involved in the reduction of inflammation.The degree of cytotoxicity of individual NPs depended on both the NP type and the used test. The most toxic to vascular endothelial cells, ZnO NPs induced a dose dependent decrease in cell viability and motility. In case of CB NPs and amorphous form of SiO2 no significant apoptosis was detected\; although a significant decrease in cell proliferation in the following days of exposure was observed. The disturbance of proper endothelial function was probable due to accumulation of NPs inside cells. Ni and ZnO NPs with positive zeta potential caused the highest percentage of damage to plasmid DNA, whereas both forms of negatively charged SiO2 NPs elicited minimal bioreactivity. Interestingly, ZnO NPs exerted DNA damage at one hundred times lower dose than the other tested NPs. Hemolytic activity was observed only in case of SiO2 NPs, especially the amorphous form. It was also demonstrated that all NPs, once in solutions, underwent aggregation and showed an instable dispersion.In summary, the results confirmed bioreactivity of airborne particles, which was demonstrated by up\-regulation of genes involved in inflammation and repair processes in both the bronchial epithelium and vascular endothelial cells. It was also shown that the same concentration of PM2.5 collected in different places produced various degrees of cytotoxicity, which strongly depended on chemical composition of particles. Experiments on different types of NPs showed that despite no immediate decrease in cell viability, NPs were able to affect normal cell function, including migration activity. Further studies are needed to elucidate various mechanisms underlying harmful effects of PM2.5 on human health."]

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