Initial organ damage due to prolonged cold storage delays graft function following implantation and has a major impact on survival of the transplanted organ. Endothelial cells are sensitive to cold ischemia-reperfusion injury which causes loss of viability and increased expression of adhesion molecules. Aim of the study was to develop a new organ protection approach to avoid the deleterious effects of prolonged cold ischemia on graft function during the early phase post transplantation. Initially, prominent apoptosis of human umbilical endothelial cells incubated for 24 h at 4°C in UW solution followed by 30 min rewarming in cell culture medium (37°C) was observed. Using PCR and Western blot analysis, a cold-induced increase in adhesion molecule VCAM-1 or CD40 expression and a simultaneous decrease in ICAM-1 expression was observed both on mRNA and protein level. Analysis of heat shock protein 70 (hsp70) expression revealed an increase which according to data in the literature may be viewed as a cellular protection mechanism. Under the aforementioned experimental conditions, activation of transcription factors AP-1, NF-kB and STAT1 was monitored by gel shift analysis. Interestingly, expression of hsp70 was further increased while that of VCAM-1 was blocked by a neutralizing STAT1 decoy oligonucleotide. Currently, signal pathways involved in cold-induced gene expression, in particular the role reactive oxygen species play therein is under investigation.