|Education||BS, Salisbury State University|
|Current Position||Postdoctoral Fellow|
Autoimmune myocarditis and inherited genetic predisposition
Autoimmune myocarditis and its sequela, dilated cardiomyopathy, are a chief cause of heart failure in individuals under 40 years old and are major reasons for heart transplant. To study the genetic and molecular factors that contribute to autoimmune myocarditis, our laboratory established a model of experimental autoimmune myocarditis (EAM) in the mouse by immunizing with cardiac myosin: B10.S mice are resistant; whereas, A.SW mice are susceptible to EAM. We have discovered a susceptibility locus on chromosome 1 (Eam1). To confirm that Eam1 has a critical role in the development or persistence of EAM in the susceptible strain, B10.S Eam1 congenic mice were induced with EAM. We found that B10.S Eam1 congenic mice develop disease, indicating that the Eam1 susceptibility locus is playing an important role in EAM.
Using the TUNEL assay, we found that lymph node cells of A.SW mice have significantly less CP-induced apoptosis and significantly less caspase 3, 8 and 9 activities compared to B10.S mice. Furthermore, we have found that lymph node cells isolated from B10.S Eam1 congenic mice have less CP-induced cell death measured by the TUNEL assay and less caspase 3, 8 and 9 activities compared to the B10.S parental strain, suggesting that Eam1 may regulate cell death. My primary focus is to understand how the Eam1 locus may be regulating cell death and EAM.