Zelieann R Craig

Zelieann R Craig

Associate Professor, Animal and Comparative Biomedical Sciences
Assistant Dean, Research
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Department Affiliations
Contact
(520) 621-8082

Work Summary

Work Summary

We investigate how the chemicals in our daily lives interact with the female reproductive system and influence fertility. We hope that our discoveries will help reduce the incidence of infertility and improve women's health.

Research Interest

Research Interest

Nearly 50 million couples experience some form of infertility worldwide. Several factors increase a woman’s risk for infertility including aging, stress, and exposure to chemicals. A group of chemicals collectively known as phthalates have been classified as endocrine disruptors based on their ability to interact with the reproductive system. Phthalates have been detected in human urine, animal tissues, and feed. Despite these observations, how phthalates interact with the female reproductive system and what this means for overall fertility is currently unknown. Dr. Craig's work focuses on understanding how phthalates affect the function of the ovary, the major reproductive organ in females. Thus, work in her laboratory is focused on using animal models to help us understand the mechanisms by which phthalates exert their effects on the ovary, 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 inspire and guide future work aimed at reducing, preventing, and/or reversing chemical-related infertility in humans and animals. Keywords: Infertility, Toxicology, Endocrine Disruptors, Phthalates, Reproduction

Publications

Barton, J. K., Connolly, D. C., Craig, Z. R., Chambers, S. K., Hutchens, G. V., Dominguez Cooks, J. P., Koevary, J. W., Howard, C. C., Rice, P. F., & Hoyer, P. (2018). Comparison of Markers of Reproductive Function in Female C57Bl/6 versus TgMISIIR-TAg Transgenic Mice: Effect of VCD exposure on Ovarian Failure.. Comparative Medicine.
BIO5 Collaborators
Jennifer Kehlet Barton, Zelieann R Craig
Craig, Z. R., Davis, J. R., Marion, S. L., Barton, J. K., & Hoyer, P. B. (2010). 7,12-Dimethylbenz[A]Anthracene Induces Sertoli-Leydig-Cell Tumors in the Follicle-Depleted Ovaries of Mice Treated with 4-Vinylcyclohexene Diepoxide. COMPARATIVE MEDICINE, 60(1), 10-17.
BIO5 Collaborators
Jennifer Kehlet Barton, Zelieann R Craig
Rivera, Z., Christian, P. J., Marion, S. L., Brooks, H. L., & Hoyer, P. B. (2009). Steroidogenic capacity of residual ovarian tissue in 4-vinylcyclohexene diepoxide-treated mice. Biology of reproduction, 80(2), 328-36.
BIO5 Collaborators
Heddwen L Brooks, Zelieann R Craig

Menopause is an important public health issue because of its association with a number of disorders. Androgens produced by residual ovarian tissue after menopause could impact the development of these disorders. It has been unclear, however, whether the postmenopausal ovary retains steroidogenic capacity. Thus, an ovary-intact mouse model for menopause that uses the occupational chemical 4-vinylcyclohexene diepoxide (VCD) was used to characterize the expression of steroidogenic genes in residual ovarian tissue of follicle-depleted mice. Female B6C3F1 mice (age, 28 days) were dosed daily for 20 days with either vehicle or VCD (160 mg kg(-1) day(-1)) to induce ovarian failure. Ovaries were collected on Day 181 and analyzed for mRNA and protein. Acyclic aged mice were used as controls for natural ovarian senescence. Relative to cycling controls, expression of mRNA encoding steroidogenic acute regulatory protein (Star); cholesterol side-chain cleavage (Cyp11a1); 3beta-hydroxysteroid dehydrogenase (Hsd3b); 17alpha-hydroxylase (Cyp17a1); scavenger receptor class B, type 1 (Scarb1); low-density lipoprotein receptor (Ldlr); and luteinizing hormone receptor (Lhcgr) was enriched in VCD-treated ovaries. In acyclic aged ovaries, mRNA expression for only Cyp17a1 and Lhcgr was greater than that in controls. Compared to cycling controls, ovaries from VCD-treated and aged mice had similar levels of HSD3B, CYP17A1, and LHCGR protein. The pattern of protein immunofluorescence staining for HSD3B in follicle-depleted (VCD-treated) ovaries was homogeneous, whereas that for CYP17A1 was only seen in residual interstitial cells. Circulating levels of FSH and LH were increased, and androstenedione levels were detectable following follicle depletion in VCD-treated mice. These findings support the idea that residual ovarian tissue in VCD-treated mice retains androgenic capacity.

Rasmussen, L. M., Sen, N., Liu, X., & Craig, Z. R. (2016). Effects of oral exposure to the phthalate substitute acetyl tributyl citrate on female reproduction in mice. Journal of applied toxicology : JAT.
Craig, Z. R., Marion, S. L., Funk, J. L., Bouxsein, M. L., & Hoyer, P. B. (2010). Retaining Residual Ovarian Tissue following Ovarian Failure Has Limited Influence on Bone Loss in Aged Mice. Journal of osteoporosis, 2010.
BIO5 Collaborators
Zelieann R Craig, Janet L Funk

Previous work showed that retaining residual ovarian tissue protects young mice from accelerated bone loss following ovarian failure. The present study was designed to determine whether this protection is also present in aged animals. Aged (9-12 months) C57BL/6Hsd female mice were divided into: CON (vehicle), VCD (160 mg/kg; 15d), or OVX (ovariectomized). Lumbar BMD was monitored by DXA and μCT used to assess vertebral microarchitecture. BMD was not different between VCD and CON at any time point but was lower (P