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
- Environ Toxicol Pharmacol. 2019 Jul;69:112-119. doi: 10.1016/j.etap.2019.04.008.
- 1. Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, 81Meishan Road, Hefei, Anhui, 230032, China.
- 2. Xuzhou Centre for Disease Control and Prevention of Jiangsu, China.
- 3. Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, 81Meishan Road, Hefei, Anhui, 230032, China. Electronic address: [email protected].
- 4. Department of Occupational Health and Environment Health, School of Public Health, Anhui Medical University, 81Meishan Road, Hefei, Anhui, 230032, China. Electronic address: [email protected].
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.