Effects of cooking oil fume derived fine particulate matter on blood vessel formation through the VEGF/VEGFR2/MEK1/2/ERK1/2/mTOR pathway in human umbilical vein endothelial cells

[Display omitted] •COF-derived PM2.5 inhibited the tube formation of HUVECs in a concentration- dependent manner.•VEGF, VEGFR2, MEK1/2, ERK1/2 and mTOR pathway was involved in the inhibitory effects.•Cell viability gradually decreased after exposure to COF-derived PM2.5. In China, cooking oil fume derived fine particulate matter (COF-derived PM2.5) is a principal source of indoor air pollution. Here, we investigated cytotoxicity of COF-derived PM2.5, as well as the roles of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR cascade in the inhibitory effects of COF-derived PM2.5, on angiogenesis in human umbilical vein endothelial cells (HUVECs). After exposure to COF-derived PM2.5, cell viability and tube formation, as well as protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR in HUVECs were measured. Cell viability and number of tubes reduced dose-dependently after COF-derived PM2.5 and SU5416 treatment. In addition, SU5416 and VEGF significantly affected tube formation. The protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR all tended to reduce with the increase of COF-derived PM2.5 concentrations. These findings demonstrate that VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR play key roles in COF-derived PM2.5 induced inhibition of angiogenesis in HUVECs.