Tissue Factor-Thrombin–PAR-1 Pathway: A Novel Link Between Bone Marrow and Blood Vessel

Abstract

Transplant arteriopathy (TA) is an important limitation to graft survival following solid organ transplantation.1 TA is a result of immune-mediated mechanisms and results in intimal hyperplasia (IH) and vascular occlusion. Our understanding of the mechanism for this process is expanding to include an important role for host derived-circulating cells, including cells that adopt a smooth muscle cell phenotype within the intima of vessels.2 In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Chen and colleagues3 add to this understanding of TA in a new and unexpected way that suggests that the tissue factor (TF)-thrombin–PAR-1 pathway may provide an important link between the bone marrow and blood vessels. See accompanying article on page 42 To further define the role of circulating cells in TA, Chen and colleagues used a model in which expression of a tethered form of tissue factor pathway inhibitor (TFPI) is driven from the α-smooth muscle actin (α-SMA) promoter. Thus, cells expressing α-SMA express this tethered protein that …