Carmen J. Williams, M.D., Ph.D.
Reproductive & Developmental Biology Laboratory / Reproductive Medicine Group
Building 101, Room E448B
111 T.W. Alexander Drive
Research Triangle Park, NC 27709
The Reproductive Medicine Group focuses on translating basic laboratory findings regarding the events surrounding the initiation of pregnancy to the clinical problem of infertility. We study the male and female gametes, how they interact with each other at fertilization, and how the newly formed embryo develops within the female reproductive tract during the first few days of life. Information gathered in these studies will provide a better understanding of factors causing human infertility, which affects approximately 10% of the reproductive age population.
Our approach is to use a mouse model to address questions of what factors are important determinants of egg and embryo quality, and what factors within the oviduct and uterus promote successful fertilization and embryo development. We are also studying how neonatal exposure to an estrogenic endocrine disruptor alters the ability of the reproductive tract environment to support fertilization and embryo development. Environmental contaminants and endocrine disruptors likely contribute to human infertility because of cumulative effects on the quality of both sperm and eggs, and their impact on the female reproductive tract environment. These problems are compounded because couples delay childbearing and therefore have longer exposure to various environmental insults. There is experimental evidence that environmental exposures can disrupt processes of oocyte growth and maturation needed to generate healthy, fertilizable eggs and embryos that are capable of full term development. Less is known regarding factors that affect sperm quality; however, environmental exposures such as alcohol use, smoking, and certain heavy metals clearly have a negative influence on sperm. We know from our studies in the mouse that phytoestrogen exposure in the neonatal period can disrupt ovarian function and causes abnormalities in the female reproductive tract that diminish the ability of the reproductive tract to support embryo development and implantation. Further work in these areas may provide insights into how endocrine disruptors and other environmental toxins can affect human fertility and reproductive tract function, and may have relevance to development of reproductive tract tumors and endometriosis.
Dr. Williams obtained her MD from Duke University School of Medicine and completed a residency in Obstetrics & Gynecology at Pennsylvania Hospital and a fellowship in Reproductive Endocrinology & Infertility at the University of Pennsylvania. She subsequently completed a PhD and postdoctoral training with Richard Schultz at Penn and joined the Penn faculty as an Assistant Professor of Obstetrics & Gynecology. She moved to the NIEHS in 2007, where she leads the Reproductive Medicine Group within the Laboratory of Reproductive and Developmental Toxicology.
Jefferson WN, Padilla-Banks E, Phelps JY, Cantor AM, Williams CJ. Neonatal phytoestrogen exposure alters oviduct mucosal immune response to pregnancy and affects preimplantation embryo development in the mouse. Biol Reprod. 2012;87(1):10, 1-10.
Miao YL, Stein P, Jefferson WN, Padilla-Banks E, Williams CJ. Calcium influx-mediated signaling is required for complete mouse egg activation. Proc Natl Acad Sci U S A. 2012;109(11):4169-74.
Bernhardt ML, Zhang Y, Erxleben CF, Padilla-Banks E, McDonough CE, Miao YL, Armstrong DL, Williams CJ. CaV3.2 T-type channels mediate Ca²⁺ entry during oocyte maturation and following fertilization. J Cell Sci. 2015;128(23):4442-52.
Jefferson WN, Chevalier DM, Phelps JY, Cantor AM, Padilla-Banks E, Newbold RR, Archer TK, Kinyamu HK, Williams CJ. Persistently altered epigenetic marks in the mouse uterus after neonatal estrogen exposure. Mol Endocrinol. 2013;27(10):1666-77.
Winuthayanon W, Bernhardt ML, Padilla-Banks E, Myers PH, Edin ML, Lih FB, Hewitt SC, Korach KS, Williams CJ. Oviductal estrogen receptor α signaling prevents protease-mediated embryo death. Elife. 2015;4:e10453.