Donald S. Torry, PhD
Dr. Torry is a Professor in the Department of Medical Microbiology, Immunology and Cell Biology, Clinical Professor of Obstetrics and Gynecology, Department of Obstetrics and Gynecology, Director of Basic Science Research for the Simmon's Cancer Institute, and Associate Dean for Research 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.
My laboratory is currently investigating two novel situations where angiogenesis is critically important; pregnancy and cancer. 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. We were the first to show that expression of the angiogenic growth factor, placenta growth factor (PlGF) is severely decreased in pregnancies complicated with preeclampsia, one of the leading causes of maternal and fetal morbidity and mortality. In spite of this clinical relevance, little is known regarding the cells and stimuli that regulate angiogenic growth factor production at the maternal-fetal interface during gestation. 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 nontrophoblast cells. How this unique and cell type specific regulation of PlGF expression is mediated is not known.
Natural killer (NK) cells in the decidua during early pregnancy associate with vessels and promote implantation and vascular remodeling highlighting the importance of these innate immune cells to facilitate successful pregnancy. Human decidua NK (dNK) cells express high levels of PlGF and vascular endothelial growth factor (VEGF) in situ. However, PlGF and VEGF expression does not occur in peripheral NK (pNK) cells. Similarly, we found conversion of pNK to dNK-like cells occurs in renal cell carcinoma. The ability of NK cells to contribute to both the physiological or pathological processes of pregnancy or tumor growth is a result of their “re-programming” that occurs within those microenvironments. Understanding the mechanisms contributing to the conversion of NK cells to pro-angiogenic dNK-like cells might provide novel approaches to limit tumor growth and/or metastasis.
General Laboratory Techniques:
Cell culture, isolation and culture of primary human trophoblast, NK cells and umbilical vein endothelial cells, real-Time PCR, qRT-PCR, RNA isolation, protein assays, Western blotting, immunoprecipitation, Flow cytometry, reporter gene assays, transient transfections, Immunohistochemistry, enzyme-linked Immunosorbant assays (ELISA), gene cloning and recombinant DNA techniques, adenovirus and lentivirus mediated gene delivery in primary human cells.