The transcription factor AP-1 is involved in apoptosis and hypertrophy in isolated ventricular cardiomyocytes (CMLs) of rats. To show the influence of AP-1 in apoptosis and hypertrophy in vivo, we analysed transgenic mice, which overexpress the AP- 1 inhibitor JDP2 heart-specific and time-dependent. In this way, we searched out if CMLs of mice are protected against an induction of apoptosis or hypertrophy by chronic and acute (1week) inhibition of AP-1. For the induction of apoptosis CMLs were incubated with TGFa1 (3ng/ml) and determined by annexin/propidium iodide staining. While TGFa1 enhanced the number of apoptotic cells of wild type (WT) mice, TGFa1 could not induce apoptosis upon chronic and acute inhibition of AP-1. As stimulus of hypertrophy we used the a-adrenoceptor agonist isoprenaline (ISO, 50 nM) and determined Cross Sectional Area (CSA). In myocytes of WT mice ISO enlarged the CSA, whereas upon chronic as well as acute inhibition of AP-1, the cell size did not increase after stimulation with ISO. In conclusion, chronic and acute JDP-2 overexpression inhibit apoptosis induced by TGFa1 and inhibit a-adrenergic stimulated hypertrophy in CMLs of transgenic mice. Thus, the inhibition of AP-1 protects against an induction of hypertrophy or apoptosis in CMLs of mice. This shows in vivo the essential role of AP-1 in both processes.