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 Vascular Microphysiological Systems to Model Genetic and Acquired Diseases
Wednesday, 19 June 2019 at 11:30
Add to Calendar ▼2019-06-19 11:30:002019-06-19 12:30:00Europe/LondonHuman Vascular Microphysiological Systems to Model Genetic and Acquired DiseasesOrgan-on-a-Chip and Tissue-on-a-Chip Europe 2019 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
Cardiovascular disease represents the major cause of death in much of the world today. Current in vitro models fail to recapitulate the complex tissue architecture and 3D structure of in vivo vasculature and animal models do not accurately model disease states. To address these limitations, we developed an endothelialized tissue engineered blood vessel (eTEBV) microphysiological system. Small-diameter eTEBVs (400-800 µm) were prepared by plastic compression and perfused at physiological shear stresses for 1- 5 weeks. The eTEBVs expressed von Willebrand factor and demonstrated endothelial cell (EC)-specific release of nitric oxide (NO). Acute stimulation by TNFa transiently inhibited ACh-induced relaxation and was eliminated by pre-exposure of eTEBVs to therapeutic doses of statins. Treatment of eTEBVs with enzyme-modified low-density lipoprotein (eLDL) caused activation of endothelial cells and promoted monocyte adhesion and transmigration. Further, treatment of eTEBVs with 50 µg/mL of eLDL for 96 hours caused monocytes to become foam cells and inhibited vasoactivity, indicators of early atherosclerosis. Monocyte accumulation and foam cell formation were inhibited by addition of lovastatin with eLDL. Using smooth muscle cells (SMCs) and ECs derived from induced pluripotent stem cells (iPSCs), we produced a functional eTEBV model of Hutchison-Gilford Progeria Syndrome (HGPS), a rare, accelerated aging disorder caused by an altered form of the lamin A (LMNA) gene termed progerin. eTEBVs fabricated with SMCs from individuals with HGPS show reduced vasoactivity, increased medial wall thickness, calcification and apoptosis in comparison to eTEBVs fabricated with SMCs from normal individuals or primary MSCs. HGPS viECs aligned with flow but exhibited reduced function compared to normal controls. Relative to eTEBVs with healthy cells, HGPS eTEBVs showed reduced function and markers of cardiovascular disease associated with the endothelium. HGPS eTEBVs exhibited a reduction in both vasoconstriction and vasodilation and HGPS viECs produced VCAM-1 and E-selectin in eTEBVs with either healthy or HGPS viSMCs. HGPS eTEBV function could be restored by addition of a farnesyl transferase inhibitor with or without a rapamycin analog. These results indicate that we can use human eTEBVs to model a variety of diseases in vitro.
Add to Calendar ▼2019-06-18 00:00:002019-06-19 00:00:00Europe/LondonOrgan-on-a-Chip and Tissue-on-a-Chip Europe 2019Organ-on-a-Chip and Tissue-on-a-Chip Europe 2019 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
Add to Calendar ▼2019-06-19 11:30:002019-06-19 12:30:00Europe/LondonHuman Vascular Microphysiological Systems to Model Genetic and Acquired DiseasesOrgan-on-a-Chip and Tissue-on-a-Chip Europe 2019 in Rotterdam, The NetherlandsRotterdam, The NetherlandsSELECTBIOenquiries@selectbiosciences.com
