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Name:	Michael E. Davis
Position:	Assistant Professor of Biomedical Engineering, Emory/GA Tech
Degree:	Ph.D., Emory University, 2003
Programs:	MSP, Full Member
Phone:	404 727-9858
Address:	2001 WMB, 101 Woodruff Circle, 1930-001-1AF
Email:	Michael.davis@bme.emory.edu
Research Descriptions:
Short:	The delivery of small molecule inhibitors and antioxidants for cardiac regeneration and stem cell therapy.
Long:	The major cause of heart failure is regional loss of myocardium following myocardial infarction. Because the loss of tissue is highly localized, and the endogenous response is not sufficient, recent efforts have focused on replacement of the lost cells using a variety of treatment options. These include, but are not limited to, cell therapy, gene therapy and biomaterial-based grafts. Gene therapy has been plagued by a variety of shortcomings including poor transfection efficiencies, inability to target specific cells and uncontrolled expression of the target gene/protein. Cell based therapies have been met with enthusiasm, however much debate still liners on the optimal delivery method of cells and exact cell type which holds the most promise. Indeed, many cells most likely diffuse away from the site of injection, making biomaterial-based grafts more feasible. These grafts, while promising have many shortcomings when combined with cell therapy including poor cell engraftment, survival and differentiation. Recently, a new phase of biomaterial design has come into favor: smart biomaterial engineering. Many studies have attempted to engineer the biomaterials to enhance the survival and retention of the cells to be implanted including modifying the biomaterials to contain adhesion sequences and loading the scaffolds with specific growth factors. Oxidative stress is greatly increased in the myocardium following infarction. The exact source of the free radical production has been examined and there are several candidates including cardiac fibroblasts, as well as invading neutrophils and myocytes. The increased superoxide following infarction not only increases damage to the local myocardium, but through dismutation to hydrogen peroxide may increase lipid peroxidation and cardiac fibrosis. Myocardial levels of the endogenous hydrogen peroxide scavenger catalase successively decrease in the weeks following infarction and its absence may also lead to incomplete regeneration by resident stem cells. Additionally, several therapies reported to improve cardiac function following infarction also increased catalase levels. Finally, oxidative stress initiates apoptosis in stem-cell derived cardiomyocytes and may play a role in the survival and efficacy of cardiac stem cells during aging. My research focuses on using biomaterials to deliver compounds to the highly vascularized myocardium that would otherwise be lost to diffusion. We currently are using polyketal particles, an exciting new class of polymers, to deliver small molecule signaling inhibitors to the myocardium to prevent fibrosis and dysfunction. We also are exmining delivery of superoxide dismutase and catalase, two important reactive oxygen species scavengers. It is our hope that we can achieve sustained inhibition or antioxidant therapy for the course of the post-infarct dysfunction and remodeling.