CVRC trainees represented the Center well at this year’s American Heart Association Basic Cardiovascular Sciences (AHA BCVS) Scientific Sessions. The conference, held July 23-26 in Baltimore, MD, is the AHA’s flagship conference for fundamental research. Among the attendees from UVA, Alex Eichert, Bryce Murillo, Julian Vitello, and Katie Pavelec, PhD, received recognition for their research. These students, mentored by Matthew Wolf, MD, PhD and Jeffrey Saucerman, PhD, presented projects related to cardiomyocytes, the heart’s muscle cells.
Eichert won an Early Career Poster Competition award, selected from amongst the conference’s 487 poster presenters. His presentation, “Growth Differentiation Factor 11 Regulates Cardiomyocyte Cycling After Myocardial Infarction,” discusses work investigating how heart muscle recovers from a heart attack. Specifically, Eichert hypothesized that cardiomyocytes release a compound, Growth Differentiation Factor 11 (GDF11), during cell division after a heart attack to prevent the muscle’s ability to contract from being lost. He showed that secreted GDF11 may prevent cell proliferation after heart attacks, which correlated to poorer heart function.
Murillo’s presentation, “Pharmacological Inhibition of DYRK1A Induces Cardiomyocyte Cell Cycle Activity,” was selected to be one of ten talks given in the Early Career sessions. He spoke about using a drug to increase the ability of cardiomyocytes to divide and proliferate, which is a limiting factor in the heart’s ability to heal after trauma. The Wolf team has previously shown that removing a particular protein, dual specificity tyrosine phosphorylation regulated kinase 1A, from the cell increases their ability to divide after a heart attack. Murillo showed that inhibiting that protein with a drug also improved the heart’s ability to heal, indicating possible future clinical applications of the drug for treating heart injuries.
Vitello’s presentation, “Wilms Tumor 1 Role in Cardiomyocyte Regeneration,” described network modeling of Wilms Tumor 1 and retinoic acid signaling in cardiomyocyte proliferation. Building on findings from the Wolf lab, she hypothesized that cardiomyocytes that re-express the transcription factor Wilms Tumor 1 are responsive to retinoic acid.
Pavelec was selected to present in the main conference sessions. These are typically populated with talks by faculty, reflecting the strength of her postdoctoral research. Her talk, “Physiological Stress and Cardiomyocyte Cycling Drive Hypertrophic Cardiomyopathy with MYBPC3 truncation mutation,” investigates the genetic origins of hypertrophic cardiomyopathy (HCM), a condition where heart muscles, particularly in the left ventricle, thickens and stiffens, resulting in poor heart function. One gene mutation is responsible for an outsized percentage of cases. Pavelec used CRISPR-based gene editing to create a mouse model with the same genetic profile as a HCM patient at UVA. The model develops symptoms like human patients – increased heart mass, increased wall thickness, and decreased circulation efficiency. Interestingly, these symptoms got worse each time the mice became pregnant. This presents the team with a possible avenue to develop therapeutics for HCM.
Congratulations, Alex, Bryce, Julian, and Katie!