Biological Sciences, UMB 2006
Area of Doctoral Study: Toxicology
Undergraduate Institute: University of Maryland, Eastern Shore
Research Advisor: Dr. Jodi A. Flaws
Current Position : Pharmacologist, Food and Drug Administration, Office of New Drug
Description of Research
My research investigates the role of the aryl hydrocarbon receptor (AhR) in the ovary. The AhR is a ligand activated transcription factor found in the cytosol of most mammalian tissues and cells. The AhR plays an important role in mediating the toxicity of several environmental contaminants. Upon binding of a ligand to the AhR, a cascade of events occurs which may lead to the induction of various metabolizing enzymes and some toxic effects. AhR deficient (AhRKO) mice have been produced to study the various biological responses mediated by the AhR. Initial studies have shown that the AhR has an important role in the female reproductive system. Investigations by Abbott et al. (1998) showed that AhRKO mice had difficulty maintaining conceptuses during pregnancy, surviving pregnancy and lactation, and rearing pups to weaning. Studies have also shown that the AhR has an important role in the mouse ovary. Normal mouse ovaries have a healthy number of primordial follicles, which first grow into primary follicles, then into pre-antral follicles, followed by the growth into antral follicles, and then finally growth into ovulatory follicles. However, studies by Benedict et al. (2000) found that AhRKO mice have a decreased number of antral follicles compared to wild-type mice (WT). Benedict et al. (2003) also found that the AhRKO mice and WT mice have the same rate of atresia (process of cells dying), which suggests that the decrease in antral follicle numbers is due to slow follicular growth and not follicle death. The reason that deleting the AhR affects follicle growth is still unknown. Based on my preliminary data showing that AhRKO mice have significantly lower levels of estradiol, my thesis work will test the hypothesis that the AhR regulates ovarian follicle growth via mechanisms involving estradiol steroidogenesis.