Professor, Vice Chair of Education, Director, Free Radicals in Medicine Program and Director, EPR Spectroscopy Core, Integrative Physiology and Molecular Medicine Doctoral Program
PhD 2004, University of Iowa
Specialty: Redox Signaling & Antioxidants; Hypertension
Major Interest: Redox signaling in normal physiological pathways and pathophysiological conditions; Delivery of nanoformulated antioxidants for the improved treatment of human diseases, particularly cardiovascular disease.
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Hypertension (high blood pressure) is a cardiovascular disease associated with increased activity of brain cells called neurons. Elevated levels of molecules called reactive oxygen species (ROS) in neurons have been shown to be involved in the development and progression of hypertension. My laboratory investigates the precise location of ROS generation in neurons and how these ROS control neuronal activation. We are particularly interested in how ROS act as signaling intermediates to regulate redox-sensitive proteins that ultimately control neuronal ion channel activity. In addition, we investigate how antioxidant enzymes work to decrease neuronal activation and lower blood pressure. In examining these unknowns, the laboratory strives to advance opportunities to develop new therapeutics that may need to be targeted to specific neuronal cell populations and/or subcellular compartments for the improved treatment of hypertension. One such new therapy that we are currently investigating, in collaboration with UNMC’s Center for Drug Delivery and Nanomedicine (CDDN), is an antioxidant protein, called superoxide dismutase (SOD), wrapped by very small polymers to make what has been called, SOD nanozyme. We have shown that SOD nanozyme is taken up by neurons resulting in increased levels of functional SOD within the cell. In addition to examining the therapeutic efficacy of SOD nanozyme in animal models of hypertension, future studies will be designed to determine if new antioxidant therapeutics can be targeted to specific subcellular compartments to decrease levels of the damaging ROS.
Link to Publications