Dr. Zelieann R. Craig is an Assistant Professor in the School of Animal and Comparative Biomedical Sciences at the University of Arizona in Tucson, AZ. Dr. Craig received her Bachelor's of Science in Industrial Microbiology from the University of Puerto Rico at Mayagüez in 2004 and her Ph.D. in Physiological Sciences from the University of Arizona in 2009. Dr. Craig completed her postdoctoral work in Reproductive Toxicology in the Department of Comparative Biosciences at the University of Illinois Urbana-Champaign where she was awarded an NIEHS Pathway to Independence Award (K99/R00). She joined University of Arizona in the Fall 2013.
Dr. Craig is interested in understanding how environmental chemicals affect the fertility of women and animals. Her current work focuses on understanding how phthalates, a group of endocrine-disrupting chemicals, affect ovarian function. Thus, work in her laboratory is focused on using animal models to elucidate the mechanisms by which phthalates exert ovarian toxicity, determine whether phthalates cause female infertility, and examine whether the effects of phthalates on female reproduction can be prevented or reversed. Using this knowledge she hopes to develop additional models to evaluate other chemicals and environmental factors that could influence both human and animal reproduction.
Because of her expertise in reproductive biology and toxicology, Dr. Craig joined the SWEHSC Southwest Hazardous Environmental Exposure Research Focus Group (RFG-1). As a new faculty member, she is currently receiving mentoring through the Career Development Core of the SWEHSC. She has already begun collaborating with SWEHSC members through a pilot project with Dr. Richard Vaillancourt which investigates how phthalates interact with cell signaling pathways in breast cancer cells and mouse mammary gland. Dr. Craig has also joined the T32 faculty and will mentor undergraduate students participating in the Environmental Health Sciences Transformative Research Undergraduate Experience (EHS-TRUE).
Publications:
Wright LE, Christian PJ, Rivera Z, Van Alstine WG, Funk JL, Bouxsein ML, Hoyer PB. Comparison of skeletal effects of ovariectomy versus chemically-induced ovarian failure in mice. J Bone Miner Res 2008; 23:1296-1303.
Rivera Z, Christian PJ, Marion SL, Brooks HL, Hoyer PB. Steroidogenic capacity of residual ovarian tissue in VCD-treated mice. Biol Reprod 2009; 80:328-336.
Craig ZR, Davis JR, Marion SL, Barton JK, Hoyer PB. 7,12-dimethylbenz[a]anthracene (DMBA) induces Sertoli-Leydig cell tumors in the follicle-depleted ovary of 4-vinylcyclohexene diepoxide (VCD)-treated mice. Comp Med 2010; 60:10-17.
Craig ZR, Marion SL, Funk JL, Bouxsein ML, Hoyer PB. Retaining Residual Ovarian Tissue following Ovarian Failure Has Limited Influence on Bone Loss in Aged Mice. Journal of Osteoporosis 2010; Article ID 157323, 6 pages.
Craig ZR, Leslie TL, Hatfield KL, Gupta RK, Flaws, JA. Mono-hydroxy methoxychlor alters levels of key sex steroids and steroidogenic enzymes in cultured mouse antral follicles. Toxicol Appl Pharmacol 2010; 249(2):107-113.
Basavarajappa MS, Craig ZR, Hernández-Ochoa MI, Paulose T, Leslie TC, Flaws, JA. Methoxychlor reduces estradiol levels by altering steroidogenesis and metabolism in mouse antral follicles in vitro. Toxicol Appl Pharmacol 2011; 253:161-169.
Craig ZR, Wang W, Flaws JA. Endocrine-disrupting chemicals in ovarian function: effects on steriodogenesis, metabolism, and nuclear receptor signaling. Reproduction 2011 Nov;142(5):633-46.
Wang W, Craig ZR, Basavarajappa MS, Gupta R, Flaws JA. Di (2-ethylhexyl) phthalate inhibits growth of ovarian antral follicles through an oxidative stress pathway. Toxicol Appl Pharmacol 2012; 258:288-295.
Paulose T, Hannon PR, Peretz J, Craig ZR, Flaws JA. Estrogen receptor alpha overexpressing mouse antral follicles are more sensitive to atresia induced by methoxychlor and its metabolites. Toxicol Appl Pharmacol 2012; 33:353-360.
Karman BN, Basavarajappa MS, Craig ZR, Flaws JA. 2,3,7,8-Tetrachlorodibenzo-p-dioxin activates the aryl hydrocarbon receptor and alters sex steroid hormone secretion in a dose dependent manner without affecting growth of mouse antral follicles in vitro. Toxicol Appl Pharmacol 2012; 261:88-96.
Peretz J, Craig ZR, Flaws JA. Bisphenol A inhibits follicle growth and induces atresia in cultured mouse antral follicles independently of the genomic estrogenic pathway. Biol Reprod. 2012; 87(3):63, 1-11.
Brannick KE, Craig ZR, Himes AD, Peretz JR, Wang W, Flaws JA, Raetzman LT. Prenatal exposure to low doses of bisphenol A increases pituitary proliferation and gonadotrope number in female offspring at birth. Biol Reprod 2012; 87(4):82, 1-10.
Wang W, Craig ZR, Basavarajappa MS, Hafner KS, Flaws JA. Mono (2-ethylhexyl) Phthalate Induces Oxidative Stress and Inhibits Growth of Mouse Ovarian Antral Follicles. Biol Reprod. 2012; 87(6):152.
Craig ZR, Hannon PR, Wang W, Ziv-Gal A, Flaws JA. Di-n-butyl phthalate disrupts the expression of genes involved in cell cycle and apoptotic pathways in mouse ovarian antral follicles. Biol Reprod 2013; 88(1) 23.
Ziv-Gal A, Craig ZR, Wang W, Flaws JA. Bisphenol A inhibits cultured mouse ovarian follicle growth partially via the aryl hydrocarbon receptor signaling pathway. Reprod Toxicol 2013; 42:58-67.
Craig ZR, Hannon PR, Flaws JA. Pregnenolone co-treatment partially restores steroidogenesis but does not prevent growth inhibition and increased atresia in mouse ovarian antral follicles treated with mono-hydroxy methoxychlor. Toxicol Appl Pharmacol 2013; 272(3):780-786.
Craig ZR, Singh J, Gupta RK, Flaws, JA. Co-treatment of mouse antral follicles with 17β-estradiol interferes with mono-2-ethylhexyl phthalate (MEHP)-induced atresia and altered apoptosis gene expression. Reprod Toxicol 2014; 45:45-51.
Sen N, Liu X, Craig ZR. Short term exposure to di-n-butyl phthalate (DBP) disrupts ovarian function in young CD-1 mice. Reprod Toxicol 2015; 53:15-22.
