We are studying the role of E-selectin in blood vessel formation, maintenance and regression in normal development, physiology and disease. Current efforts focus on angiogenesis and antiangiogenesis in inflammation, wound healing and cancer. This work began as a long-term collaboration with Dr. Joyce Bischoff of Children's Hospital Boston.

We have shown that E-selectin is required for the antiangiogenic action of endostatin in vivo . Current studies focus on the cell biologic and molecular mechanisms mediating this interaction, the significance of these mechanisms more broadly in other settings of blood vessel formation and regression, and the significance of E-selectin expression in specifying sensitivity and resistance to endostatin's antitumor action. 

Previous studies of E-selectin-deficient mice, created in our laboratory in collaboration with Dr. Michael Gimbrone and studied in collaboration with Drs. Jain, Melder, Fukumura and Monsky at Massachusettes General Hospital, also identified an obligate role for E-selectin in firm adhesion of leukocytes to activated endothelium lining blood vessels, an important process during transmigration at sites of acute inflammation.