Matthew C. Zimmerman

Matthew C. Zimmerman


Assistant Professor
Ph.D. 2004, University of Iowa
Specialty: Free Radical Biology
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.

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Recent Publications:
  1. Yin JX, Yang RF, Li S, Renshaw AO, Li YL, Schultz HD, Zimmerman MC. Mitochondria-produced Superoxide Mediates Ajngiotensin II-induced Inhibition of Neuronal Potassium Current. Am J Physiol Cell Physiol. 2010; 298(4):C857-65. *Highlighted in April 2010 issue of Physiology.  PMID: 20089930
  2. Rosenbaugh EG, Roat JW, Gao L, Yang RF, Manickam DS, Yin JX, Schultz HD, Bronich TK, Batrakova EV, Kabanov AV, Zucker IH, Zimmerman MC. The Attenuation of Central Angiotensin II-dependent Pressor Response and Intra-neuronal Signaling by Intracarotid Injection of Nanoformulated Copper/Zinc Superoxide Dismutase. Biomaterials. 2010; 31(19):5218-26. PMID: 20378166
  3. Yi X, Zimmerman MC, Yang RF, Vinogradov S, Kabanov AV. Pluronic-modified Superoxide Dismutase 1 (SOD1) Attenuates Angiotensin II-induced Increase in Intracellular Supoxide in Neurons. Free Radical Biol Med. 2010; 49(4):548-58. PMID: 20493251
  4. Yang RF, Yin JX, Li YL, Zimmerman MC*, Schultz HD*. Angiotensin-(1-7) Increases Neurjonal Potassium Current via a Nitric Oxide-dependent Mechanism. Am J Physiol Cell Physiol. 2j011; 300(1):C58-64. *Contributed equally as corresponding author. PMID: 20980550
  5. Zimmerman M.C. Angiotensin II and angiotensin-1-7 Redox Signaling in the Central Nervous System. Curr Opin Pharmacol. 2011; 11(2):138-43. PMID: 21257347