George Truskey,
R. Eugene and Susie E. Goodson Professor of Biomedical Engineering,
Duke University
George Truskey is the R. Eugene and Susie E. Goodson Professor and Senior Associate Dean for Research in the Pratt School of Engineering. Dr. Truskey's research interests include cardiovascular tissue engineering, microphysiological systems, and the mechanisms of atherogenesis. He also studies cell adhesion and cell biomechanics, for which he focuses upon the effect of flow on endothelial cell adhesion to synthetic surfaces and monocyte adhesion to endothelium. He received a PhD degree in 1985 from MIT. He has been a faculty member in the Department of Biomedical Engineering at Duke since 1987. From 2003-2011, he was Chair of the Department of Biomedical Engineering at Duke University. He is the author of over 110 peer-reviewed research publications, a biomedical engineering textbook entitled Transport Phenomena in Biological Systems, six book chapters, over 180 research abstracts and presentations, 1 patent and 2 patent applications. He is a Fellow of the Biomedical Engineering Society (BMES), the American Institute of Medical and Biological Engineering, and the American Heart Association. He was president of BMES from 2008 to 2010. He received the Capers and Marion McDonald Award for Excellence in Mentoring and Advising from the Pratt School of Engineering at Duke (2007) and the BMES Distinguished Service Award (2012).
Circulatory System and Integrated Muscle Tissue for Drug and Toxicity Testing
We have developed functional human tissue-engineered blood vessels (TEBVs) and skeletal muscle myobundles that model normal structure and function and represent disease states. We have fabricated specialized perfusion systems for the human TEBVs and skeletal muscle myobundles that enable in situ measurements of vasoactivity, dimensions, leukocyte adhesion, calcium transients, contractile force and oxygen uptake. Offline measurements include glucose uptake, nitric oxide production, gene and protein expression, and metabolite levels. These microphysiological systems (MPS) have been prepared using primary human cells, induced pluripotent stem cells (iPSCs) from human fibroblasts, and reprogrammed endothelial cells. Disease states that we examined including inflammation, Duchenne Muscular Dystrophy (DMD), metabolic storage disease, and Hutchison-Gilford Progeria Syndrome (HGPS). Since iPSC-derived cells exhibit reduced function relative to primary cells, addition of small molecules that activate specific transcription factors controlling differentiation improves MPS function. We have generated an immortalized human primary DMD cell line to prepare functional myobundles. The bundles show some characteristics of a dystrophic muscle such as increased susceptibility to repeated eccentric contractions, evidence of myotube branching, and potential hypercontraction of myotubes. TEBVs prepared with cells from HGPS patients exhibit reduced numbers of smooth muscle cells, apoptosis and calcification, conditions found in vessels of adults with the disease. Treatment of TEBVs with cells derived from HGPS patients with rapamycin appears to improve TEBV function.
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