Angiogenesis is a tightly regulated process known to be essential for normal embryonic development that is implicated in physiological, as well as, pathological phenomena in fully developed organisms. Although stimulation of new blood vessel growth has been proposed as a therapeutic approach to treat certain disorders, an excessive and deregulated angiogenic response is thought to contribute to cancer, diabetic retinopathy, arthritis and psoriasis. Therefore, several anti-angiogenic agents have been developed to be used as effective treatments in angiogenesis-related disorders. In the present study, we have investigated the effects of poly (ADP-ribose) polymerase (PARP) inhibition on angiogenesis. PARP is a DNA-repair enzyme that also regulates transcription by affecting histones, DNA methylation and enhancer/promoter regions. In order to investigate potential effects of PARP on angiogenesis we have utilised the selective PARP inhibitor, PJ-34 [N-(6-Oxo-5,6-dihydro-phenanthridin-2-yl)-N,N-dimethylacetamide], which is currently evaluated in human clinical trials for neurodegenerative diseases and ischemia reperfusion-induced tissue injury. Treatment of chicken chorioallantoic membranes (CAM) with PJ-34 reduced vascular length in these tissues; paradoxically, lower doses of PJ-34 (0.03 or 0.3 nmol/egg) were more effective in inhibiting neovascularization than higher doses (3 or 30 nmol/egg). In vitro, incubation of endothelial cells (EC) with PJ-34 (300 nM to 10 μΜ concentration) inhibited their proliferation in a concentration-dependent manner; maximal inhibition of 22.3 % was observed at 10 μM. Capillary morphogenesis on matrigel was also negatively affected by PJ-34. Moreover, PJ-34 (300 nM) abolished the migratory response to the prototype angiogenic factor, vascular endothelial growth factor (VEGF). In conclusion, we provide evidence that PARP inhibition reduces EC proliferation, migration and organization leading to decreased angiogenesis.