RESUMO
Atmospheric particulate matter (PM2.5) is associated with the morbidity and mortality of cardiovascular diseases. However, whether PM2.5 penetrates into the cells and the potential mechanisms are unknown. Hence, the study firstly indicated that PM2.5 could penetrate into the HUVEC cells, and phagocytosis, micropinocytosis, caveolin as well as clathrin mediated the internalization of PM2.5 into HUVEC cells. Particularly, the components of PM2.5-Metal, PAHs and WSC could enter into HUVEC cells mainly via the micropinocytosis, clathrin and caveolin mediated endocytosis, respectively. The current data of environmental assessments indicated that PM2.5-Metal were extremely harmful to the ecological environment and human health. Moreover, accompanying with mitochondrial fusion gene Mfn1 was increased and fission genes Opa1 and Drp1 were decreased, and the lysosome related genes LAMP2 and LAMP3 were decreased, the phenomenon that the morphology of mitochondrial and lysosome injured was observed in HUVEC cells treated with PM2.5 and/or PM2.5-Metal. These data suggest that PM2.5 and its main components depend on different endocytosis penetrate into HUVEC cells and cause the mitochondrial and lysosomal damages. Thereby, our study provides the potential mechanism of haze particles penetration into HUVEC cells and damage to organelles.
