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).
Human Microphysiological System of Arteriole Scale Blood Vessels for Disease Modeling and Toxicity Testing
We have developed an endothelialized tissue engineered blood vessel (eTEBV) microphysiological system by rapid generation of small-diameter vessels (400-800 µm inner diameter) by plastic compression. For the medial cell layer, we used human neonatal dermal fibroblasts (hNDFs), mesenchymal stem cells (hMSCs), induced pluripotent stem cells (iPSCs), or SMCs derived from hiPSCs. TEBVs were mechanically strong enough to allow endothelialization and perfusion at physiological shear stresses immediately after fabrication. eTEBVs perfused at physiological shear stresses for 1- 5 weeks expressed von Willebrand factor (vWF) and demonstrated EC-specific release of NO, indicating a confluent layer of ECs. After 1-5 weeks of perfusion, eTEBVs exhibited dose-dependent contraction and relaxation following exposure to phenylephrine and acetylcholine (ACh), respectively. In contrast, TEBVs without ECs or eTEBVs pre-treated with the NO synthase inhibitor L-NG-Nitroarginine methyl ester underwent vasoconstriction in response to ACh consistent with vasodilation by EC release of NO. TEBVs elicited reversible activation by acute stimulation by TNFa which transiently inhibited ACh-induced relaxation, and was eliminated by pre-exposure of eTEBVs to therapeutic doses of statins. Using smooth muscle cells derived from iPSCs, we produced a functional three-dimensional model of Hutchison-Gilford Progeria Syndrome (HGPS) is a rare, accelerated aging disorder caused by an altered form of the lamin A (LMNA) gene termed progerin. eTEBVs fabricated with smooth muscle cells from individuals with HGPS show reduced vasoactivity, increased medial wall thickness, increased calcification and apoptosis in comparison to eTEBVs fabricated with smooth muscle cells from normal individuals or primary MSCs. In addition, treatment with the rapamycin analog, RAD001, for one week increases HGPS TEBV vasoactivity. These results indicate that we can use human eTEBVs to model diseases in vitro. This work was supported by NIH grants UH2TR000505, 4UH3TR000505, and the NIH Common Fund for the Microphysiological Systems Initiative.
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