ABSTRACT
Because EC loss plays a pivotal role in the pathogenesis of intimal hyperplasia after vascular injury, it is postulated that a therapeutic strategy that promotes early reendothelialization of the injured vessels would inhibit intimal lesion development, facilitate vascular repair, and improve long-term vessel patency. Opportunities to enhance reendothelialization include delivery of agents that directly or indirectly stimulate native EC proliferation and migration. Alternatively, direct delivery
of harvested autologous ECs has been proposed. Technical concerns in harvesting mature ECs and their senescence has limited the direct delivery of mature ECs. This concept of direct delivery of ECs has been bolstered by the identification of cells originating from the bone marrow capable of assuming an endothelial phenotype. 5,6 These cells have high proliferative potential and, under specific growth conditions, differentiate into ECs, 7,8 suggesting that they may be suitable as a substrate for the reendothelialization of damaged vessels.
