Matthew C. Zimmerman
Matthew C. Zimmerman

Associate Professor & Vice Chair, and Director, Integrative Physiology and Molecular Doctoral Program
Ph.D. 2004, University of Iowa
Specialty: Free Radical Biology; Hypertension
Major Interest: Role of reactive oxygen species produced in neuron Mitochondria in the pathogenesis of hypertension; Delivery of nanoformulated superoxide dismutase (SOD) protein to central neurons
Curriculum Vitae

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 mitochondrial-produced ROS and how these signaling intermediates regulate redox-sensitive proteins that ultimately control neuronal ion channel activity. In addition, we investigate how antioxidant enzymes in neurons may 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.

Recent Publications:
  1. Case A.J. and Zimmerman M.C. Sympathetic-mediated activation versus suppression of the immune system: Consequences for Hypertension. J Physiol. 2016; 594(3):527-36. doi: 10.1113/JP271516. PMCID: PMC4930069. PMID: 26830047
  2. Ahmad I.M., Temme J.B., Abdalla M.Y., Zimmerman M.C. Redox status in workers occupationally exposed to long term low levels of ionizing radiation: A pilot study. Redox Report. 2016; 21(3):139-45. doi: 10.1080/13510002.2015.1101891. PMCID: PMC5011313.  PMID: 26817988
  3. Collister J.P., Hartnett C., Mayerhofer T., Nahey D., Stauthammer C., Kruger M., Tobias A., O’Sullivan G., Parker J., Tian J., Case A.J., Zimmerman M.C. Overexpression of copper/zinc superoxide dismutase in the median preoptic nucleus improves cardiac function after myocardial infarction in the rat. Clin Exp Pharmacol Physiol. 2016; 43(10):960-6. DOI: 10.1111/1440-1681.12607. PMCID: PMC5008989. PMID: 27297082.
  4. Case A.J., Roessner C.T., Tian J., Zimmerman M.C. Mitochondrial superoxide signaling contributes to norepinephrine-mediated T-lymphocyte cytokine profiles. PLoS One. 2016; 11(10):e0164609. doi: 10.1371/journal.pone.0164609. PMCID: PMC5058488.  PMID: 27727316
  5. Case A.J., Tian J., Zimmerman M.C. Increased mitochondrial superoxide in the brain, but not periphery, sensitizes mice to angiotensin II-mediated hypertension. Redox Biol. 2017; 11:82-90. DOI: 10.1016/j.redox.2016.11.011. PMCID: PMC5124355.  PMID: 27889641