Director of Physiological Environment Research Facility
Ph.D. 2011, The University of Iowa
Specialty: Redox biology and immunology
Major Interest: Redox signaling and function of T-lymphocytes during psychological-stress induced cardiovascular disease.
The generation of free radicals and reactive oxygen species was long thought to be nothing more than a detrimental and damaging process to cells. In recent years, this dogma has shifted and it is now appreciated that the redox environment is essential to normal cellular functioning and signaling. The overarching theme of my research is to examine the role of the redox and metabolic environment in regulating T-lymphocyte function in models of psychological stress.
The term psychological stress encompasses a broad spectrum of disorders ranging from generalized anxiety to post-traumatic stress disorder (PTSD). While these conditions have well-characterized psychological manifestations, often overlooked are the physiological changes to the rest of the body. It has been shown that patients suffering from PTSD have increased risk for both immune disorders and cardiovascular diseases. Our working hypothesis is that these secondary maladies stem from dysfunctional autonomic nervous system function due to the stressing condition. More specifically, we believe an over-abundance of norepinephrine (NE) from the sympathetic nervous system modifies the immune system to be auto-reactive and pro-inflammatory. Understanding the molecular pathways involved in this process may elucidate innovative targets in the immune system that may help treat these secondary diseases, and may also improve psychological function in these patients as well.
- Case, AJ.*, Roessner, CT., Tian, J., and Zimmerman, MC. Mitochondrial superoxide signaling contributes to norepinephrine-mediated T-lymphocyte cytokine profiles. (2016) PLoS ONE. 11(10): e0164609. PMCID: PMC5058488. PMID: 27727316 *Corresponding author
- Case, AJ., Tian, J., and Zimmerman, MC. Increased mitochondrial superoxide in the brain, but not periphery, sensitizes mice to angiotensin II-mediated hypertension. (2017) Redox Biology. 11:82-90. PMCID: PMC5124355. PMID: 27889641
- Case, AJ. and Zimmerman, MC. Sympathetic-mediated activation versus suppression of the immune system: consequences for hypertension. (2016) J Physiol. 594(3):527-36. PMCID: PMC4930069. PMID: 26830047
- Case AJ, Zimmerman MC. Redox-regulated suppression of splenic T-lymphocyte activation in a model of sympathoexcitation. (2015) Hypertension. 65(4):916-23. PMCID: PMC4359089. PMID: 25691620
- Case, AJ, Li S, Basu U, Tian J, Zimmerman MC. Mitochondrial-localized NADPH oxidase 4 is a source of superoxide in angiotensin II-stimulated neurons. (2013) Am J Physiol Heart Circ Physiol. 305(1):H19-28. PMCID: PMC3727106. PMID: 23624625
*Highlighted article and interview for American Journal of Physiology Heart and Circulatory Physiology podcast, July, 2013.