In response to pressure-overload, the myocardium exhibits a complex molecular changes, characterized by the reexpression of a fetal phenotypes. Although signaling pathways involved in these changes are still largely unknown, studies on the differential expression of the myosin heavy chain (MHC) genes will provided a framework for understanding the molecular mechanisms underlying the reprogramming of cardiac gene expression in response to mechanical load. Recently, in vitro medel of myocardial stretch on the silicone sheet has demonstrated the up regulation of the "cardiac fetal genes", including beta-MHC, skeletal alpha-actin, and atrial natriuretic factor (ANF), which is known to be a hallmark of the altered gene expression in the hypertrophic heart. Transient transfection experiments using this model will be useful for identifying the "stretch-response element" within the promoters of these genes. Furthermore, this approach will eventually identify the stretch-induced intracellular pathways.