Pictured above: A 3D render of the stretcher platform. Cells are seeded in the square translucent reservoir and then stretched over the period of several days.
Hypertrophic cardiomyopathy (HCM) is the result of abnormal thickening of the ventricular walls and an increased tissue stiffness within the heart, leading to a reduction in the ability of this critical organ to pump blood. In an effort to allow a better understanding of the disease, we are first developing a model which will serve to emulate HCM in an in-vitro setting. By stretching an elastomeric membrane for a prolonged period of time to simulate the stiffening of the myocardial tissue, we hope to better identify patterns in calcium dynamics and sarcomere function that represents this diseased phenotype. As this is my ongoing project more information will be available soon!
Pictured Below: Example videos of cardiomyocytes in culture. The left video outlines the contractile abilities of the cells. The right serves to demonstrate the influx of calcium into the cell and triggers a fluorescent protein. Both of these properties will be evaluated to determine the effectiveness of the model.
Above: Immunostained image revealing F-Actin structure within cardiomyocytes on a PDMS substrate. Image taken at 10x magnification.
Below: A-C depict the formation of F-Actin stress fibers formed upon mechanical stretching of cardiomyocytes. D-F display the cytoskeletal structure of the non-stretched group cultured on PDMS. Images taken at 40x magnification. F -Actin stained in green, cardiac troponin-T stained in red.
