The expression pattern of angiotensin AT2 receptors with predominance during 
fetal life and upregulation under pathological conditions during tissue 
injury/repair process suggests that AT2 receptors may exert an important action 
in injury/repair adaptive mechanisms. Less is known about AT2 receptors in acute 
ischemia-induced cardiac injury. We aimed here to elucidate the role of AT2 
receptors after acute myocardial infarction. Double immunofluorescence staining 
showed that cardiac AT2 receptors were mainly detected in clusters of small 
c-kit+ cells accumulating in peri-infarct zone and c-kit+AT2+ cells increased in 
response to acute cardiac injury. Further, we isolated cardiac c-kit+AT2+ cell 
population by modified magnetic activated cell sorting and fluorescence 
activated cell sorting. These cardiac c-kit+AT2+ cells, represented 
approximately 0.19% of total cardiac cells in infarcted heart, were 
characterized by upregulated transcription factors implicated in cardiogenic 
differentiation (Gata-4, Notch-2, Nkx-2.5) and genes required for self-renewal 
(Tbx-3, c-Myc, Akt). When adult cardiomyocytes and cardiac c-kit+AT2+ cells 
isolated from infarcted rat hearts were cocultured, AT2 receptor stimulation in 
vitro inhibited apoptosis of these cocultured cardiomyocytes. Moreover, in vivo 
AT2 receptor stimulation led to an increased c-kit+AT2+ cell population in the 
infarcted myocardium and reduced apoptosis of cardiomyocytes in rats with acute 
myocardial infarction. These data suggest that cardiac c-kit+AT2+ cell 
population exists and increases after acute ischemic injury. AT2 receptor 
activation supports performance of cardiomyocytes, thus contributing to 
cardioprotection via cardiac c-kit+AT2+ cell population.