Inhalation of diesel exhaust particles (DEPs) is associated with pulmonary and
cardiovascular disease. One contributor to pathogenesis is inhaled particles reaching and
injuring the lung capillary endothelial cells, and possibly gaining access to the blood stream.
Using in vitro capillary tubes as a simplified vascular model system for this process, it was
previously shown that DEPs induce the redistribution of vascular endothelial cell-cadherin
(VE-Cad) away from the plasma membrane to intracellular locations. This allowed DEPs into …