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The Levinson Emerging Scholars Program
Kate Buckley - Bioengineering
Kate Buckley’s strong interest in cardiac repair began when she was introduced to the field by her mentor, Dr. Mike Regnier. Kate has been passionate about research since she arrived in the lab in the fall of her freshman year, and is motivated by a continuing interest in the therapies she investigates and the constant need for translational research that aims to address current health problems. Kate is particularly interested in creating genetic and cellular therapies in cardiac muscle that could be applied to different types of heart disease. The Levinson Scholarship has given her the opportunity to explore a novel research question that will allow her to delve deeper into the exciting opportunities that research offers.
In addition to research, Kate enjoys traveling and being actively involved in the Bioengineering program and the Honors Program. Kate is an avid learner and is constantly seeking new applications for her training as a bioengineer and research scientist.
After graduating, Kate plans to attend graduate school to continue her work with cardiac repair. She aims to one day perform clinically applicable research and teach students in the field of bioengineering and physiology.
Mentor: Mike Regnier, Bioengineering
Project Title: Gene therapy and the adrenergic response: L48Q cTnC virally transduced adult cardiomyocytes.
Abstract: Heart disease is the leading cause of death in the United States. After a heart attack (one of the most common results of heart disease), the heart undergoes an extensive remodeling process when normal cardiovascular function is disrupted. At the University of Washington exciting new therapeutic strategies are being developed to that improve and repair heart function. Gene based therapies that target cardiac myofilaments offer a way to halt or even reverse this process by altering contractile properties of the heart. Genetic transfer of the mutant L48Q troponin C offers potential as a therapeutic tool to improve function of surviving myocardium by enhancing Ca 2+ triggering of contraction. However, if this therapy is to be useful following an infarct, it must allow the ability for the heart to respond to adrenergic stimulation under stress. This project will investigate the adrenergic response of infarcted and non-infarcted myocardium with L48Q cTnC transfection into the myofilaments. Using cultured adult rat heart cells, the levels of adrenergic stimulation will be varied and the response characterized by measuring the changes in contraction and relaxation parameters. Contraction measurements will be made on individual cardiomyocytes using video microscopy coupled to computer software that measures cell and sarcomere length changes. After completing studies in cultured cardiomyocytes, this study will extend to an animal model of gene transfection to study the effect of L48Q cTnC and the adrenergic response at the in vivo and whole organ level. These studies are essential to determine if this gene therapy has the potential to be clinically relevant and reduce changes leading to heart failure. If so, L48Q cTnC has great potential as a therapeutic tool for several forms of cardiac disease.