[en] The full text of the publication follows. The dysfunctions of the endothelium are clearly involved in early and late pathologies induced by radiotherapy [1]. Senescence, one of the alternative becoming of cells after radiation, is defined by cell cycle blockage and also by an increase of metabolic activity. Senescence presents therapeutic benefits by lowering the tumor progression and drawbacks by inducing vascular dysfunctions. Molecular pathways inducing radiation-induced senescence remain unclear, but may involve the generation of reactive oxygen species and the induction of DNA damage. Previously, our team describes a differential endothelial death response in function of the dividing cell status. Proliferating cells died after exposure to ionizing radiation through either a Ceramide generation-induced pre-mitotic apoptosis or a DNA damage-induced mitotic death. Non-dividing cells keep the ability to die by the ceramide-induced apoptosis, but not mitotic death. In fact, sphingosin-1-Phosphate, inhibitor of ceramide-dependent signaling pathway, blocks death of quiescent, but not proliferating endothelial cells [2]. However, consequences of DNA damage and their potential roles remain to be clarified. In consequence, our hypothesis is that remaining DNA-damage provokes radio-induced senescence on quiescent endothelial cells, which comprise the vascular functions in healthy tissues. This hypothesis will be verified by underlining X-rays-induced senescence in vitro (HUVEC and HMVEC-L) and in vivo (mouse and patient) on quiescent endothelial cells using Senescence-associated β-Galactosidase staining. Next, the involvement of ceramide and DNA-repair pathways in senescence progression will be explored. References: [1] Milliat F, et al. Role of endothelium in radiation-induced normal tissue damages. Ann Cardiol Angeiol. 2008; 57: 139-148. [2] Bonnaud S, et al. Sphingosine-1-Phosphate Protects Proliferating Endothelial Cells from Ceramide-Induced Apoptosis but not from DNA Damage-Induced Mitotic Death. Cancer Res. 2007; 67: (4): 1803-1811. (authors)