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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

From: Platelet activation independent of pulmonary inflammation contributes to diesel exhaust particulate-induced promotion of arterial thrombosis

Fig. 6

Diesel exhaust particles alter the endogenous fibrinolytic system in HUVECs. Human umbilical vein endothelial cells were exposed to diesel exhaust particles (DEP; 100 μg/ml, 16 h, black columns) or vehicle (white columns) then incubated in the presence or absence of thrombin (1.0 U/ml, 24 h). Pre-exposure to DEP reduced expression of (i) tissue plasminogen activator (t-PA) and (ii) plasminogen activator inhibitor (PAI-1). Exposure to DEP (150 μg/ml; 6–24 h) also reduced (iii) t-PA antigen concentrations and (iv) PAI-1 activity in culture media. Stimulation with thrombin did not significantly increase t-PA antigen levels in media (v) but increased PAI-1 activity (vi). Thrombin-stimulated PAI-1 activity was suppressed in cells pre-incubated with DEP. Data are mean ± s.e.mean (n = 6). Comparisons were made using Student’s unpaired t-test; **P < 0.01, ***P < 0.001

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