| 초록 |
Significant structural remodeling is observed in most of the heart diseases such as hypertrophy, ischemic cardiomyopathy, and heart failure. Gross structural change of the heart chamber is directly reflected at the cellular level by altering the morphology of individual cardiomyocytes. However, the relationship between cardiomyocytes shape and the mechanical dysfunction is still unknown. Utilizing traction force microscopy combined with the cell patterning technique, we analyzed systolic stress of cardiomyocytes as a function of cell shape. We found that cardiomyocyte contractility is optimized at the cell length to width ratio observed in normal hearts, and decreases in cardiomyocytes with morphologies resembling those isolated from failing hearts. Quantitative analysis of sarcomeric architecture revealed that the change of contractility may arise from alteration of myofibrillar structure. We also measured intracellular calcium in myocytes with varied aspect ratios and found that calcium transients decayed slowly in cells with high aspect ratios. Our data suggest that myocyte shape is critical in determining pumping performance of the ventricular wall by regulating the intracellular structure and calcium handling ability. The study for single myocytes is extended into a micro cardiac tissue consisting of a pair of cardiomyotyes. |
