Presentation description

Humans lack a robust mechanism to resolve scarring caused by an injury to the heart. After cardiac damage like a myocardial infarction, commonly known as a heart attack, humans form a non-contractile scar that impairs contractility and function of this dynamic organ. In contrast, some species of fish and amphibians can clear cardiac scarring and regenerate damaged tissues allowing them to maintain their cardiac function. Zebrafish, a species with robust cardiac regenerative capabilities, have been recognized as a crucial model to help us understand the differences between species that can and cannot regenerate their hearts. Through exploring these differences, we can begin to identify pathways that promote healing. Significant cardiac regeneration research on zebrafish has utilized a model of injury that mimics a myocardial infarction where a lesion of necrotic tissue and a subsequent scar is formed; however, we have not adequately explored how the regenerative capabilities of zebrafish may protect the heart from forming a scar in the first place. In this project, I explore zebrafish's ability to resist damage from a modeled bacterial infection. Injection of bacterial cell wall proteins has been used as a way to model systemic infections and has been found to cause non-regenerating species to form fibrotic tissue in the heart; however, when zebrafish are injected with the same proteins, they turn on pro-regenerative pathways. I hypothesize that this ability to turn on this regenerative cascade protects zebrafish from significant fibrosis. To explore this hypothesis, I injected zebrafish and Japanese medaka, a similar teleost species that cannot regenerate its heart, with a bacteria lipoprotein and used various tools to understand the cardiac response. Through continuing this work, I can begin to explore cardioprotective features that could also protect humans from scar formation.