Training:

1983 B.S. Southern Illinois University, Carbondale, IL
Biology/Chemistry Education
1985 M.A. Southern Illinois University
Carbondale, IL
Microbiology/Immunology
1989 Ph.D. Southern Illinois University
Carbondale, IL
Microbiology/Immunology
1989-1992 Postdoctoral Research Fellow
Department of Pathology, Harvard Medical School and
Division of Molecular Genetics,
Dana-Farber Cancer Institute
Boston, MA

Research Focus
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.

Selected Publications
Welch P, Miller P, Amankwah K, Miller P, McAsey M and Torry DS. Correlations placenta perfusion and PlGF expression in early human pregnancy. American Journal of Obstetrics and Gynecology, 194(6):1625-1629, 2006.

Petroff MG, Kharatyan E, Torry DS and Holets L. The novel members of the extended B7 family are differentially expressed across gestation in the human placenta. American Jourrnal of Pathology 167(2):465-473, 2005.

Torry DS, Hinrich M, and Torry RJ. Determinants of placental vascularity. American Journal of Reproductive Immunology 51:257-268, 2004.

Arroyo J, Torry RJ and Torry DS. Differential regulation of placenta growth factor (PlGF)-mediated signal transduction in human primary term trophoblast and endothelial cells. Placenta 25:379-386, 2004.

Torry DS, Arroyo J, Mukherjea D, and Torry RJ. Function of placenta growth factor: Implications for abnormal placentation. J Society for Gynecologic Investigation, 10:178-188, 2003.