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The Levinson Emerging Scholars Program

Jacqueline Robinson-Hamm - Bioengineering

Jacqueline Robinson-HammJacqueline was forced to end her gymnastics career early due to a rare degenerative bone disease in her right elbow. However, investigations into the disease and lack of treatment inspired her to pursue bioengineering. Her passion lies in novel ways to treat disease. She joined Dr. Regnier’s Heart and Muscle Mechanics laboratory sophomore year, inspired by the ongoing work to address the loss of function post heart attack. The rich and supportive environment has helped her develop greatly as a scientist. Senior year she is collaborating with Dr. Marcinek's Translational Center for Metabolic Imaging to investigate a novel gene therapy to treat loss of function in skeletal muscle. She plans to attend graduate school and earn her PhD in bioengineering. Following graduate school, she hopes to gain a faculty position at a top research institution and continue in meaningful research, as well as teach to help train the next generation of bioengineers.

Mentor: Michael Regnier, Bioengineering

Project Title: Performance characterization of cardiac and skeletal muscle with increased 2-deoxy-ATP

Abstract: Cardiovascular disease and skeletal muscle disease that result in loss of contractile function affect people around the world. Current heart disease therapies aid in slowing the progression of heart failure, but there are no treatments that restore healthy cardiac function short of transplant. Dr. Regnier's laboratory is pursuing a novel treatment for heart disease that will prevent the progression of heart failure by restoring cardiac function to healthy levels. The laboratory has discovered that a nucleotide analog of ATP, 2-deoxy-ATP (dATP), which is produced in cardiomyocytes, greatly improves cardiac performance. The Regnier laboratory has studied the effect of increased dATP concentration in cardiomyocytes in both transgenic animals that overexpress the enzyme that catalyzes dATP formation, ribonucleotide reductase (R1R2), and in cells virally modified to have R1R2 overexpression. In both models, the therapeutic effect of increased dATP concentration was observed: cells with increased dATP concentration have an increased rate and magnitude of contraction, and an increased rate of relaxation. To further the study, I will be initiating collaboration with Dr. David Marcinek's laboratory to explore the effects of dATP in skeletal muscle in transgenic mice. Twitch, tetanus, and fatigue protocols will be conducted on both in vivo and in vitro skeletal muscle from wild type and transgenic mice that overexpress R1R2. The combined findings from both laboratories will help complete the characterization of how increased dATP concentration affects muscle and whether upregulation of this nucleotide might be beneficial in treating skeletal muscle disease as well as cardiac disease.