Professor of Pharmacology
Obstetrics and Gynecology
- Reproductive Science Research
Primary Office: 2-530 Bowen Science Building
Iowa City, IA 52242
Primary Office Phone: 319-335-9907
Lab: 2-505 Bowen Science Building
Iowa City, IA 52242
Web: More information
BS, Biochemistry, San Carlos University, Guatemala
PhD, Biochemistry, Vanderbilt University, Nashville, TN
Post Doctoral, Department of Biochemistry, M.D. Anderson Hospital and Tumor Institute, The University of Texas, Houston, TX
Education/Training Program Affiliations
Biosciences Graduate Program
Receptors and Signal Transduction / Cellular and Molecular Endocrinology
The lutropin/choriogonadotropin (LHR) and follitropin (FSHR) receptors are the principal regulators of reproduction in humans. Loss-of-function and gain-of-function mutations of these receptors are known to be associated with a number of disorders of the reproductive system such as ovarian dysgenesis, ovarian hyperstimulation syndrome, Leydig cell hypoplasia, male-limited precocious puberty and Leydig cell tumors. The cognate hormones, lutropin/choriogonadotropin (LH/CG) and follitropin are widely used in the treatment of infertility.
Research in my laboratory is driven by the hypothesis that the binding of agonist to the LHR and the FSHR result in the activation of multiple signaling pathways, and that these pathways, either alone or in combination, stimulate the proliferation and differentiated functions of their respective target cells (Leydig and Granulosa cells).
Some of the projects that we are currently working on are as follows. (1) Examine the involvement of G protein-dependent and G protein-independent pathways on the LHR and FSHR-induced activation of mitogenic signaling cascades. (2) Characterize the involvement of the MEK/ERK signaling cascades on the proliferation and differentiation of Leydig cells. (3) Characterize the involvement of Gq/11 cascades on the actions of LHR in the ovary.
Experimental systems used in my laboratory include a Leydig tumor cell line, primary cultures of granulosa or Leydig cells and mice with target cell specific deletions of MEK or Gq/11.
Sequence variants in oxytocin pathway gnees and preterm birth: A candidate gene association study.
BMC Med Genet.
2013 July 26. 14:77.
Ovulation involves the luteinizing hormone-dependent activation of Gq/11 in granulosa cells.
The ERK1/2 pathway regulates testosterone synthesis by coordinately regulating the expression of steroidogenic genes in Leydig cells.
Mol. Cell Endocrinol.
The Leydig cell MEK/ERK pathway is critical for maintaining a functional population of adult Leydig cells and for fertility.
2011 April 28. 25(7):1211-1222.
Reactive oxygen species (ROS) play a critical role in the cAMP-induced activation of Ras and the phosphorylation of ERK1/2 in Leydig cells.
Transactivation of the epidermal growth factor receptor is involved in the lutropin receptor-mediated down-regulation of ovarian aromatase expression in vivo.
2010 January 21. 24(3):552-560.
Activation of the lutropin/choriogonadotropin receptor inhibits apoptosis of immature Leydig cells in primary culture.
2009 April 30. 150(8):3766-3773.
The luteinizing hormone receptor-activated extracellularly regulated kinase-1/2 cascade stimulates epiregulin release from granulosa cells.
2008 July 24. 149(11):5549-5556.
A co-culture system reveals the involvement of intercellular pathways as mediators of the lutropin receptor (LHR)-stimulated ERK1/2 phosphorylation in Leydig cells.
Exp Cell Res.
2008 July 17. 314(1):25-37.
Arrestin-3 is essential for the activation of Fyn by the luteinizing hormone receptor (LHR) in MA-10 cells.
2008 June 19. 20(10):1822-1829.
Date Last Modified: 07/31/2013 -