Author Description

Ischemic cardiomyopathy is a leading cause of mortality in North America. Although advances in current treatments have been significant in improving myocardial perfusion, many patients still cannot be treated properly. Thus, new therapies need to be developed. Since angiogenesis occurs naturally in the female reproductive tract, the cells from the uterine tissue may be ideal candidate cells to induce angiogenesis, which could be further enhanced through estrogen stimulation. My in vitro dose-response and time course demonstrated that estrogen did not regulate vascular endothelial growth factor (VEGF) protein levels in cultured uterine cells. However, an in vivo study demonstrated that transplantation of cells with or without estrogen increased blood vessel formation. The data suggests that signals mediated by cells and/or estrogen may induce larger vessel formation.