ELCACT/BME Faculty Candidate Seminar: Alison Schroer Vander Roest, Ph.D., Stanford University
Cardiac mechanobiology: Modeling altered cardiac biomechanics across scales to understand mechanisms of disease
Abstract: Many forms of cardiac disease, including myocardial infarction (MI) and hypertrophic cardiomyopathy (HCM), are characterized by changes in contractile function and tissue stiffness. Myofibroblast activation contributes to fibrotic tissue remodeling in many cardiac conditions, especially after MI, and is affected by changes in tissue mechanics and interactions with other cardiac cells. In my Ph.D. studies, I found that therapeutic targeting of a cadherin expressed in myofibroblasts and inflammatory cells after MI limits harmful remodeling. In my postdoc, I have studied how HCM mutations with surprising and variable effects on myosin function lead to hypercontractility, cytoskeletal disruption, and hypertrophy on the cellular scale and in patients. Using hiPSC-CMs, engineered cell platforms and computational models, I have linked measured changes in molecular and cellular biomechanics, probed sources of cellular variability and identified mechanisms of hypercontractility. My research leverages engineering tools to clarify the mechanical and biological mechanisms of cardiac disease and potential therapies.
Bio: Alison Schroer Vander Roest received her undergraduate and Ph.D. degrees in BME at the University of Virginia and Vanderbilt University, respectively. In her doctoral work with Dave Merryman, she studied fibroblast mechanobiology and the role of cadherin-11 in fibrotic and inflammatory remodeling after myocardial infarction. Schroer Vander Roest then pursued postdoctoral training at Stanford University co-mentored by Beth Pruitt, Jim Spudich and Dan Bernstein aiming to understand mechanisms linking mutations in beta-cardiac myosin to phenotypes of hypertrophic cardiomyopathy using stem cell models, engineered environments and computational modeling.