Dr. Herbert Weissbach
, Center for Molecular Biology and Biotechnology Associate Director and Distinguished Research Professor in the Biological Sciences Department, has received a three-year National Eye Institute research grant totaling $442,560 for a project entitled "Activators of MsrA and MsrB: potential use for diseases of the retina." This project has a number of collaborators from the Jupiter Life Science Initiative and FAU College of Medicine and Department of Chemistry and Biochemistry. Dr. Daphna Sagher, Research Associate Professor in the Weissbach laboratory, Dr. Predrag Cudic, Professor of Chemistry and Biochemistry, Dr. Maciej Stawikowski, Assistant Scientist in the Department of Chemistry and Biochemistry, and Dr. Wen Shen, Associate Professor of Biomedical Science, are all part of this collaborative research grant investigating potential treatments for retinal diseases.
Dr. Weissbach's major research interest has been in the role of oxidative damage in aging and age-related diseases, and more specifically the mechanisms that cells use to protect against oxidative damage. His laboratory discovered the methionine sulfoxide reductase (Msr) system that can repair oxidative damage to proteins resulting from methionine oxidation. The Msr system has now been shown to be involved in life span extension in both flies and worms. Small molecule activators of recombinant mammalian MsrA and MsrB have now been identified that are being tested in cell culture and animals in vivo. Recent work in his laboratory has focused on sulindac, a known NSAID, in protecting cells against oxidative damage. The Msr system reduces sulindac, a prodrug, to sulindac sulfide the active COX inhibitor. However, sulindac has novel properties unrelated to its NSAID activity. It can initiate a protective preconditioning mechanism in normal cells similar to that observed in ischemic preconditioning. As example his research has shown protection of the heart against ischemia/reperfusion damage and the retina against chemical oxidation and UV damage. Of interest is the finding that cancer cells, unlike normal cells, are more sensitive to oxidative damage after treatment with sulindac.
