Presenter: Justine Nguyen
Faculty Mentor: Kryn Stankunas, Kate Karfilis
Presentation Type: Poster 79
Primary Research Area: Science
Major: Human Physiology
Cardiomyopathies are congenital heart diseases that affect the heart musculature, which could cause the heart to become weaker and pump less blood efficiently. The purpose of my research is to study the developmental programs that underlie ventricular trabeculation and the role vascular endothelial growth factor (VEGF) plays in regulating this process. VEGF plays a distinct role in direct signaling of angiogenesis along with the cardiac muscle formation and trabeculation in the ventricles. If the gene pathways for the development of trabeculation in the heart are understood, then in a disease state, appropriate remedies could be determined based on where the genes are expressed incorrectly. Currently, two possible hypotheses could explain VEGF signaling and its role in trabecular development. One hypothesis is that VEGF signaling is directly turning on a gene that directs VEGF signaling while the other hypothesis is that the two cell types (endocardial and myocardial cells) are directly interacting with each other due to VEGF signaling. In order to study trabecular development, pregnant mice are dissected when the embryos are developing the trabeculations. Embryos are processed so that their hearts are examined through various cellular biology techniques. A specific small molecule inhibitor, Cabozantinib is used in order to inhibit VEGF signaling, disrupting the formation of the trabeculae. A VEGF inhibited sample can be compared to an untreated wildtype sample to compare the differences in the trabeculation development.