Donald S. Torry, PhD
Dr. Torry is a Professor and Chairman in the Department of Medical Microbiology, Immunology and Cell Biology, Clinical Professor of Obstetrics and Gynecology and Director of Basic Science Research for the Simmon's Cancer Institute in the Department of Obstetrics and Gynecology at SIU School of Medicine. He has served as a member of the International Federation of Placental Associations, the Society for the Study of Reproduction and the American Society for Reproductive Immunology for which he has served as Secretary (1996-2000), Treasurer (1999-2002) and President (2002-2006). He was a member of the Pregnancy and Perinatology Study Section at the National Institutes of Health, Bethesda, MD., and sits on the Editorial Boards of the American Journal for Reproductive Immunology and the Journal of Reproductive Immunology.
One of the most important adaptations to pregnancy is the intense vascular growth and remodeling associated with development of a competent placenta. Adequate vascular development and perfusion of the placental bed is essential for normal pregnancy and vascular deficiencies contribute to many obstetrical complications. In spite of this clinical relevance, little is known regarding angiogenic growth factor production by trophoblast during gestation and the molecular regulation or cellular responses of the trophoblast to angiogenic growth factors. My laboratory is currently investigating the novel angiogenic growth factor, placenta growth factor (PlGF), and its receptor (flt1) as potential regulators of trophoblast function and vascularity during pregnancy. Our previous findings show that expression of PlGF is negatively regulated in placental trophoblast by hypoxia. However, PlGF expression is readily induced by low oxygen tension in other non trophoblast cells. Whether this unique and cell type specific regulation of PlGF expression is mediated at the transcriptional and/or post transcriptional levels is not known. Primary human trophoblast also express the PlGF-specific receptor, flt-1, and exogenous PlGF induces stress activated signal transduction responses which function to protect the cells from apoptosis. These studies may be clinically important because we, and several other groups, have found that expression of PlGF is severely decreased in pregnancies complicated with preeclampsia. Thus, aberrant production of PlGF by trophoblast could influence vascular endothelium as well as trophoblast function, both of which contribute significantly to the pathophysiology of perfusion compromised pregnancies.
General Laboratory Techniques:
Cell culture, primary human trophoblast and human umbilical vein endothelial cell isolation and culture, Real-Time PCR, qRT-PCR, RNA isolation, protein assays, Western blotting, Immunoprecipitation, Reporter gene assays (β-Galactosidase, Renilla & Firefly luciferase), transient transfections, Immunohistochemistry, Enzyme-linked Immunosorbant assays (ELISA), Cloning and recombinant DNA techniques, adenovirus and lentivirus mediated gene delivery in primary human cells.