Up-regulation of Tissue Factor in Human Pulmonary Artery Endothelial Cells after Ultrafine Particle Exposure

• DOI: 10.1289/ehp.9556
• Publication Date: 2007-01-08T17:41:39Z
• Authors: Edward D. Karoly; Zhuowei Li; Lisa A. Dailey; Xhevahire Hyseni; Yuh-Chin T. Huang
• Keywords: Ultrafine particle; HMOX1; Endothelial Dysfunction

Epidemiology studies have linked exposure to pollutant particles increased cardiovascular mortality and morbidity, but the mechanisms remain unknown.We tested hypothesis that ultrafine fraction of ambient would cause endothelial cell dysfunction.We profiled gene expression human pulmonary artery cells (HPAEC) exposed (UFPs; 100 microg/mL) from Chapel Hill, North Carolina, or vehicle for 4 hr with Affymetrix HG U133 Plus 2.0 chips (n = each).We found 320 up-regulated genes 106 down-regulated (p < 0.01, 5% false discovery rate). We noted up-regulation related coagulation [tissue factor (F3) II receptor-like 2 (F2RL2)] differential regulation F3 signaling (FOS, JUN, NFKBIA). Results quantitative polymerase chain reaction show a significant after 10 microg/mLUFP exposures. Additionally, water-soluble fractions UFPs were sufficient induce F3, F2RL2, heme oxygenase 1 (HMOX1). Treatment HPAEC 16 release interleukin (IL)-6 IL-8. Pretreatment blocking antibody against attenuated IL-6 IL-8 by 30 70%, respectively.Using profiling, we discovered may vascular express clotting. These results indicate PM adverse health effects activating coagulation-inflammation circuitry.