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Effect of Polystyrene Microplastics on Tube Formation and Viability of Endothelial Cells
Summary
Lab experiments found that polystyrene microplastics impaired the ability of human endothelial cells (which line blood vessels) to form tube-like structures and reduced cell viability at higher concentrations. This is early evidence that microplastics entering the bloodstream may damage vascular cells, with potential implications for cardiovascular health.
Environmental contamination by plastics has become a concern in a wide range of fields; in particular, alarm has risen concerning exposure of human tissues to microplastics (MPs). Despite the fact that MPs cross biological barriers and enter the circulation system, no research has yet explored whether MPs impact the normal function of endothelial cells. The objective is to investigate the adverse vascular events by polystyrene microplastics (PS-MPs), focusing on tube formation and viability, using human umbilical vein endothelial cells (HUVECs). Tube formation (angiogenesis) was examined using an in vitro angiogenesis assay kit in HUVECs treated for 6 h with different doses of PS-MPs in a range of sizes (0.5, 1.0, 5 µm). Western blotting was performed to observe changes in protein expression of angiogenesis-regulating signaling components in HUVECs treated with 0, 40, and 80 µg/mL of 0.5 µm PS-MPs for 6 h. Next, we performed the MTT assay in the cells treated with different doses and sizes of PS-MPs to examine if long-term treatment with PS-MPs affects cell viability. We also examined if PS-MPs influence autophagy in HUVECs. Tube formation was inhibited by treatment with 0.5 µm PS-MPs in a dose-dependent manner and similar inhibitory activity was observed for both smaller particle sizes (0.5 and 1.0 µm) but not the large size (5 µm). The results of western blotting indicate suppression of cell migration- and angiogenesis-regulating signaling pathways (phosphorylation of p38, Smad2, Src, FAK, PLC1γ, ERK). For MTT assay, significant suppression of cell viability was observed in cells treated with 0.5 and 1 µm PS-MPs for two and three days. Regarding autophagy analysis, PS-MPs induced conversion of LC2-I to LC3-II in HUVECs treated with 0.5 µm PS-MPs. This data proposes autophagy as a possible cell death mechanism in HUVECs exposed to PS-MPs. Our data propose adverse effect of PS-MPs on the function of endothelial cells. Cooperative Agreement from USDA-ARS to University of Maryland (S-HL).