Karen Gould, PhD

Professor & Vice Chair for Faculty Development

   

Department of Genetics, Cell Biology and Anatomy
985805 Nebraska Medical Center
Omaha, NE 68198-5805

402-559-2456
Email


Education:
PhD, University of Wisconsin-Madison, 1996
M.Ed. University of Illinois-Chicago, 2020

Academic Appointments:
Assistant Dean for Graduate Student Success, UNMC Graduate Studies
Campus Director of Assessment, UNMC Academic Affairs
Deputy Research Integrity Officer, UNMC Academic Affairs
Vice Chair for Faculty Development, Department of Genetics, Cell Biology and Anatomy

Honors & Awards:
Impact in Education Award, UNMC, 2019
Interprofessional Academy of Educators, UNMC, 2018
Distinguished Graduate Mentor Award, UNMC, 2014

Teaching: 
Dr. Gould teaches genetics, cell biology, physiology, histology, and critical evaluation of the scientific literature in the graduate curriculum.  In addition, she teaches anatomy, histology, and embryology in the medical curriculum. She also contributes to graduate education by training, mentoring, and advising graduate students in multiple graduate programs. Dr. Gould also teaches in the Responsible Conduct in Research Training Workshop for graduate students. In addition to teaching students in and out of the classroom and laboratory, Dr. Gould also serves as a mentor for multiple faculty both in and outside of the department. In her role as chair of the GCBA faculty development committee and departmental promotion and tenure committee, Dr. Gould provides career and professional development support for faculty and guidance in the planning and preparation of all promotion- and tenure-related materials. Dr. Gould is a member of the Interprofessional Academy of Educators and a regular speaker at professional development seminars and workshops on campus, including those sponsored by the Office of Faculty Development and UNMC Graduate Studies. 

Research: 
Estrogen receptor alpha regulation of lupus.
Lupus is a devastating autoimmune disease that is associated with considerable morbidity and mortality. Approximately 90% of patients with lupus are women. This dramatic sex bias is due to endogenous estrogens. Using a mouse model of lupus, we have shown that estrogens promote lupus via estrogen receptor alpha (ER-alpha), which acts in a B cell intrinsic manner to enhance B cell activation and loss of tolerance.  However, a concrete understanding of how ER-alpha signaling modulates B cell activation and loss of tolerance on a molecular level is unclear.  Our current studies use genetics as well as molecular and cellular biological approaches to understand how ER-alpha impacts B cell biology and the development of lupus.

Publications listed in PubMed

Publications:
  1. Graham, J. H., Yoachim, S. D., & Gould, K. A. (2020). Estrogen Receptor Alpha Signaling Is Responsible for the Female Sex Bias in the Loss of Tolerance and Immune Cell Activation Induced by the Lupus Susceptibility Locus Sle1bFrontiers in immunology11, 582214.
  2. Tabor, D. E., & Gould, K. A. (2017). Estrogen receptor alpha promotes lupus in (NZB×NZW)F1 mice in a B cell intrinsic manner. Clinical immunology (Orlando, Fla.)174, 41–52. 
  3. Nelson, R. K., & Gould, K. A. (2016). An Lck-cre transgene accelerates autoantibody production and lupus development in (NZB × NZW)F1 mice. Lupus25(2), 137–154. 
  4. Yoachim, S. D., Nuxoll, J. S., Bynoté, K. K., & Gould, K. A. (2015). Estrogen receptor alpha signaling promotes Sle1-induced loss of tolerance and immune cell activation and is responsible for sex bias in B6.Sle1 congenic mice. Clinical immunology (Orlando, Fla.)158(2), 153–166.
  5. Yuan, F., Tabor, D. E., Nelson, R. K., Yuan, H., Zhang, Y., Nuxoll, J., Bynoté, K. K., Lele, S. M., Wang, D., & Gould, K. A. (2013). A dexamethasone prodrug reduces the renal macrophage response and provides enhanced resolution of established murine lupus nephritis. PloS one8(11), e81483. 
  6. Bynoté, K. K., Hackenberg, J. M., Korach, K. S., Lubahn, D. B., Lane, P. H., & Gould, K. A. (2008). Estrogen receptor-alpha deficiency attenuates autoimmune disease in (NZB x NZW)F1 mice. Genes and immunity9(2), 137–152.