J. Koudy Williams, DVM
Professor of Pathology (Comparative Medicine) and Surgical Sciences (General Surgery); Institute for Regenerative Medicine
Estrogens, Endothelium, Atherosclerosis
The purpose of our research is to determine the influence of certain atherosclerosis risk factors and hormones on vascular reactivity. We use cynomolgus monkeys as a nonhuman primate model of atherosclerosis in human beings. Our studies focus on two primary areas:
The Influence of Atherosclerosis on Endothelial Dysfunction as Related to Vasomotion.
Atherosclerosis has been shown to damage endothelial cells, perhaps by modifying their response to circulating vasoactive substances, resulting in altered vasomotion and vasospasm. Vasospasm can contribute to transient ischemia in several organ systems (e.g. heart, brain, eye, legs, and gut). It is known that women receiving postmenopausal estrogen replacement therapy have a decreased incidence of myocardial ischemia. The goals of this research are to determine the effect of estrogen on altered vasomotion (in vivo) and release of endothelium-derived relaxing factor (EDRF) in coronary and iliac artery segments of female cynomolgus monkeys in vitro. In addition, we are studying the effect of atherosclerosis on flow-mediated and receptor-mediated dilation in iliac arteries of cynomolgus monkeys.
The Pathobiology of Restenosis After Angioplasty in Nonhuman Primates.
Restenosis is the most common reason for coronary angioplasty to fail. The pathogenesis of restenosis is poorly understood. This is partially due to lack of a good animal model of restenosis. Studies in our laboratory focus on the effects of mammalian and plant estrogens on restenosis and the potential role of gene transfer in prevention of restenosis in a monkey model of diet-induced atherosclerosis.
Link to PubMed Database