Effect Of Cardiotrophin-1 (CT-1) On Expression Of Rat's Cardiac Transcription Factor GATA4

Background and Objective:Cardiac hypertrophy is one of the important adaptive responses for an increased demand on the heart. In this process, cardiac hypertrophy is characterized by an increase in cell size and protein synthesis and reactivation of the fetal gene program. Because cardiomyocytes are terminally differentiated and lose their ability to proliferate soon after birth. So, cardiomyocytes grow in cell size without cell division to adapt to a demand for an increased workload. Prolongation of this process will lead to heart failure at last.Cardiotrophin-1 (CT-1) was isolated in a search for new factors that induce cardiac hypertrophy by Pennica in 1995. It is a new member of the IL-6 family of cytokines that exert their biological effects through the shared signaling subunit gp130 and can activate a distinct form of myocardial cell hypertrophy that is characteristic of volume overload cardiac hypertrophy at the molecular, morphological, and cellular levels. Furthermore, it has been shown to be capable of promoting survival of ventricular muscle cells. Chronic volume overload hypertrophy can result in an irreversible loss of cardiac function. On a single cell level, dilated hypertrophic hearts exhibit an increase in cell length, reflecting the addition of new sarcomeric units in series, while concentric hypertrophic hearts display an increase in cell diameter with the addition of new myofibrils in parallel. A number of growth factors, includingα-adrenergic agonists, endothelin 1, and angiotensinⅡwhich can result concentric hypertrophy are mainly activate signals through G-protein-dependent or ras-dependent pathways. Although it has long been accepted that three are distinct morphologic forms of hypertrophy in the setting of pressure or volume...