Studies in ventricular cardiomyocytes (CMs) of rat have shown that AP-1 is involved in apoptosis and hypertrophy.We investigated, if CMs of mice, overexpressing the AP-1 inhibitor JDP-2, are protected against hypertrophy or apoptosis. To stimulate hypertrophy CMs were incubated with phenylephrine (PE) or isoprenaline (ISO). Cross sectional area (CSA) of myocytes was taken as parameter for hypertrophic growth. PE didn´t increase CSA of CMs from wildtype (WT) mice. ISO enhanced CSA in CMs from WT mice but not in CMs from JDP-2 mice. To stimulate apoptosis CMs were exposed to TGFb1. Number of apoptotic cells was determined by annexin/propidium iodide staining. In CMs from WT mice TGFb1 enhanced number of apoptotic cells significantly. In CMs from JDP-2 overexpressing mice TGFb1 didn´t induce apoptosis. In conclusion,AP-1 is a mediator of apoptosis and hypertrophy in CMs,since both processes are inhibited in mice overexpressing the AP-1 inhibitor JDP-2. Beside, we observed CMs of mice don´t respond to a-adrenergic growth stimulation, in contrast to rats. These facts may be of great importance for analyses of transgenic mouse models.