Department of Reproductive Medicine

Kellie Breen Church

Kellie Breen Church, PhD
Assistant Professor
Division of Reproductive Endocrinology

Lab Telephone:
(858) 534-1762
(858) 534-1438
Administrative Assistant:
Ruth Montouri (858) 534-1140
Visit our site at: Breen Church Lab

Education and Training

University of Michigan, Ann Arbor, MI
Ph.D. in Molecular & Integrative Physiology, 2004

University of Michigan, Ann Arbor, MI
Postdoctoral Fellow, 2004-2006

University of California, San Diego, CA.
Postdoctoral Fellow, 2007 - 2011

University of California, San Diego, CA.
Project Scientist, 2011 -2013


Hormone Action, Biology 226: Stress and Adrenal Pathophysiology

Clinical Foundations Problem Based Learning Group, UCSD Medical School

Professional Activities

Member, Endocrine Society HPA axis session Chair, ENDO 2013

Member, Women in Endocrinology Communications Committee 2013-present

Member, Association for Women in Science

Ad hoc Reviewer, Biology of Reproduction, Journal of Animal Science, Stress, Toxicology and Applied Pharmacology, Physiology and Behavior

Honors and Awards

2009    Invited Editorial, Expert Review of Endocrinology and Metabolism,
4:295-298, 2009 "Glucocorticoids: Do they really contribute to stress-related
reproductive inhibition?"

2010-2016    NIH K99/R00 Pathway to Independence Award, NICHD

2012    UCSD Health Science Senate Research Award

2013    Invited Speaker, NICHD SCCPIR Research Meeting, May 2013

Professional Membership/Service

2013-present    Member, UCSD Reproduction Journal Club Steering Committee

2011-present    Faculty Mentor, UCSD Biological Sciences Integrated BS/MS Program and Individual Research for Undergraduates (BISP 199)

2011-present    Member, UCSD Center for Reproductive Science and Medicine

2011-present    Member, UCSD/UCLA Diabetes and Endocrinology Research Center (DERC)

General Area of Interest

The impact of stress on reproduction in modern society can lead to unwanted cycle disruption and infertility. As an example, functional hypothalamic amenorrhea (FHA) is an anovulatory condition of mixed origin resulting from decreased GnRH drive and reduced pulsatile gonadotropin secretion. FHA has been attributed to stress, especially psychosocial stress, and is associated with hypothalamic-pituitary-adrenal axis activation and enhanced glucocorticoid secretion. Glucocorticoids have long been considered to be potential mediators of stress-induced suppression of ovarian cyclicity; however, the mechanisms involved are not well understood. We are interested in understanding the role of glucocorticoids in mediating reproductive neuroendocrine suppression during episodes of stress.

Recent Publications

Breen KM, Mellon PL. Influence of Stress-Induced Intermediates on Gonadotropin Gene Expression in Gonadotrope Cells. Molecular and Cellular Endocrinology. In Press. 2013.

Lindaman LL, Yeh DM, Xie C, Breen KM, Coss D. Phosphorylation of ATF2 and Interaction with NFY Induces c-Jun in the Gonadotrope. Molecular and Cellular Endocrinology 365:316-26, 2013.

Breen KM, Thackray VG, Hsu T, Mak-McCully RA, Coss D, Mellon PL. Stress levels of glucocorticoids inhibit LH-beta subunit gene expression in gonadotrope cells. Molecular Endocrinology 26:1716-1731, 2012.

Breen KM, Thackray VG, Coss D and Mellon PL. Runt-related transcription factors impair activin induction of the follicle-stimulating hormone beta-subunit gene. Endocrinology, 151:2669-2680, 2010.

Wagenmaker ER, Breen KM, Oakley AE, Tilbrook AJ and Karsch FJ. The estrous cycle of the ewe is resistant to disruption by repeated, acute psychosocial stress. Biology of Reproduction, 82:1206-1215, 2010.

Oakley AE, Breen KM, Tilbrook AJ, Wagenmaker ER and Karsch FJ. Role of estradiol in cortisol-induced reduction of luteinizing hormone pulse frequency. Endocrinology, 150:2775-2782, 2009.

Wagenmaker ER, Breen KM, Oakley AE, Tilbrook AJ and Karsch FJ. Psychosocial stress inhibits amplitude of gonadotropin-releasing hormone pulses independent of cortisol action on the type II glucocorticoid receptor. Endocrinology, 150:762-769, 2009.
*Featured in Endocrine News, A publication of the Endocrine Society, November 2008.

Breen KM, Davis TL, Doro LC, Nett TM, Oakley AE, Padmanabhan V, Rispoli LA, Wagenmaker ER and Karsch FJ. Insight into the neuroendocrine site and cellular mechanism by which cortisol suppresses pituitary responsiveness to GnRH. Endocrinology, 149:767-773, 2008.

Breen KM, Oakley AE, Pytiak AV, Tilbrook AJ, Wagenmaker ER and Karsch FJ. Does cortisol acting via the type II glucocorticoid receptor mediate suppression of pulsatile luteinizing hormone secretion in response to psychosocial stress? Endocrinology, 148:1882-1890, 2007.

Breen KM and Karsch FJ. Stress, glucocorticoids and reproductive suppression. Frontiers in Neuroendocrinology, 27:233-245, 2006.

Stackpole CA, Clarke IJ, Breen KM, Turner AI, Karsch KJ and Tilbrook AJ. Sex difference in the suppressive effect of cortisol on pulsatile secretion of luteinizing hormone in sheep. Endocrinology, 147:5921-5931, 2006.

Breen KM, Billings HJ, Wessinger EW, Wagenmaker ER and Karsch FJ. Endocrine basis for disruptive effects of cortisol on preovulatory events. Endocrinology, 146:2107-2115, 2005.

Breen KM, Stackpole CA, Clarke IJ, Pytiak AV, Tilbrook AJ, Wagenmaker ER, Young EA and Karsch FJ. Does the type II glucocorticoid receptor mediate cortisol-induced suppression in pituitary responsiveness to gonadotropin-releasing hormone? Endocrinology, 145:2739-2746, 2004.

Breen KM and Karsch FJ. Does cortisol inhibit pulsatile LH secretion at the hypothalamic or pituitary level? Endocrinology, 145:692-698, 2004.