The transcription factor p53 regulates cell cycle and apoptosis via gene activation or inhibition [ 1 ]. P53 impairs the angiogenic process by deregulation of VEGF [2], Pifithrin-alpha (PFT) is described as an inhibitor of p53 dependent gene activation [3]. Using in vivo fluorescence microscopy we examined whether the inhibition of p53 by PFT influences the angiogenic process induced by freely transplanted ovarian follicles. Ovarian follicles were isolated from PMSG-stimulated Syrian golden hamsters and transplanted in dorsal skinfold chambers of synchronized female hamsters treated daily with either 0,9% saline (control), 100% DMSO (2 µl/g bodyweight each; solvent control) or PFT (2 mg/kg bodyweight). Take rate, revascularized follicular tissue area, microvessel density, diameter of the newly formed capillaries and RBC velocity (VRBC) were assessed during two weeks following transplantation. Take rate of transplanted follicles was 100% in the saline group (n = 12), 72% in the DMSO group (n = 18) and 78% in the PFT group (n =18). Characteristic signs of revascularization were seen at day 3 in all groups. Complete microvas-cular networks were observed at day 7 in all groups with a reduced microvascular density in the DMSO and PFT group compared to the saline group. Diameters of the newly formed microvessels were significantly larger in the PFT and DMSO groups (12.0 - 17.9 µm and 11.5-17.3 µm; 25% -75% quartile) when compared to the saline group (10.5 - 14.8 µm). These inter-group differences were observed until day 14, however without being statistically significant. Thus, we conclude that in this model of ovarian follicle transplantation inhibition of p53-dependent processes did not stimulate physiological angiogenesis. However, effects of PFT on physiological angiogenesis can not be fully excluded, since DMSO per se has effects on cell cycle arrest [4] and may inhibit angiogenesis