Heart failure is a growing epidemic in the U.S. affecting nearly 6.5 million American adults (1). There are few options for treating heart failure, and additional research is needed to elucidate the pathology of heart failure at the level of the cardiomyocyte. Recently, our lab has demonstrated that loss of the critical t-tubule scaffolding protein cardiac bridging integrator 1 (cBIN1) plays a role in diabetic heart failure progression, while the exogenous reintroduction of cBIN1 rescued both heart function and proper systemic glucose handling. Since metabolic heart disease is marked by the accumulation of cytotoxic lipids like ceramides, we decided to evaluate whether an overabundance of C2 ceramides affects the expression of BIN1 isoforms.
In this project, we incubated an immortalized strain of rat embryonic cardiomyocyte cells called H9C2 with purified C2 ceramide and evaluated the expression of BIN1 isoforms. We incubated the cells with ceramides for 24 hours and after lysis utilized Western Blot to determine changes to expression levels of the four cardiac BIN1 isoforms (BIN 1, BIN1+13 17, BIN1 13, and BIN1 1 17.). As a baseline for comparison, we also determined the expression levels of the isoforms in untreated H9C2 cells.
The results are not available yet.