Director of Hypoxia Core
Ph.D. 2011, The University of Iowa
Specialty: Redox biology and immunology
Major Interest: Redox signaling and function of T-lymphocytes during hypertension
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 environment in regulating T-lymphocyte function in models of hypertension.
Hypertension is a complex disease involving numerous organ systems including the vasculature, kidneys, and brain. A common link to all of these tissues is the immune system, which has been implicated as a key mediator of blood pressure regulation. My work focuses primarily on the interaction between the brain and the immune system during hypertension. More specifically, I am attempting to elucidate how the enhanced sympathetic drive observed in hypertension affects T-lymphocyte function. Our current research suggests that the autonomic nervous system regulates T-lymphocyte function by redox signaling. Understanding the molecular pathways involved in this process may elucidate innovative targets in the immune system that may be applicable to diseases of increased sympathoexcitation, like hypertension.
- Case AJ, Agraz D, Ahmad IM, Zimmerman MC. Low-Dose Aronia melanocarpa Concentrate Attenuates Paraquat-Induced Neurotoxicity. Oxid Med Cell Longev. 2016; 2016:5296271. PMID: 26770655
- 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.
- Basu U, Seravalli J, Madayiputhiya N, Adamec, J, Case AJ, and Zimmerman MC. Rapid metabolism of exogenous angiotensin II by catecholaminergic neuronal cells in culture media. (2015) Physiol Rep. 3(2):e12287. PMCID: PMC4393196.
- Case, AJ, Domann, FE. Increased mitochondrial superoxide protects against p53 mediated tumor formation. (2014) Redox Biol. 2:220-224. PMCID: PMC3909777.
- 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.
*Highlighted article and interview for American Journal of Physiology Heart and Circulatory Physiology podcast, July, 2013.