Joyce Bischoff's work has contributed to a greater understanding of the role of endothelial cells in angiogenesis. Endothelial cells line the interior of the heart and all of the blood vessels of the body. New endothelial cells are needed for growth of organs and tissue, and also to maintain a healthy vasculature. The source of these new endothelial cells was long thought to be from pre-existing blood vessels, but new studies clearly demonstrate that their progenitors—the cells that differentiate into endothelial cells—are present in the bone marrow and in the bloodstream. Her laboratory is looking at endothelial progenitor cells in two contexts: their role in the development and regression of hemangiomas—tumors that occur in infants—and their potential use in repairing cardiovascular defects.

Hemangiomas can grow rapidly, causing organ damage, disfigurement, and even threatening life, though they usually start to regress after the child's first birthday. The Bischoff laboratory is homing in on the cellular and molecular mechanisms that drive this uncontrolled growth and spontaneous regression. Recently, they identified endothelial progenitors in proliferating hemangiomas—the first demonstration of these cells in a human vascular tumor.

Bischoff and colleagues are also studying how these cells grow and differentiate—a process that involves the molecules TGF-2 and VEGF—in the endothelium of normal heart valves. They have shown that endothelial progenitor cells can be isolated from a small sample of blood taken drawn from a person's arm and used to create tiny blood vessels. They hypothesize that endothelial progenitor cells, expanded in the lab, can be nudged into behaving as valve endothelial cells. If so, they may be used to repair cardiovascular abnormalities, including valve defects.

Bischoff's lab is also looking at E-selectin, a molecule produced by endothelial cells that has been implicated in angiogenesis. They have examined the relationship between endostatin and E-selectin, and their results indicate that E-selectin is required for the anti-angiogenic activity of endostatin. In laboratory cultures, it appears to work by making human endothelial cells responsive to endostatin. Bischoff proposes that measuring a patient's E-selectin levels may be a way to predict how well endostatin will work in anti-angiogenic therapy.