Hepatic endothelial cell function in the assessment of graft viability after liver transplantation and modification of donor MHC antigens by antisense gene transfer to prevent rejection of transplanted organs

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1.In our first study, we investigated the mechanism of cold ischemia-reperfusion injury, especially the relationship between sinusoidal endothelial cell (SEC) function and graft viability after liver transplantation. According our results, graft failure after cold ischemia-reperfusion primarily resulted from SEC damage, leading to decreased sinusoidal blood flow. Hepatocellular ischemic necrosis might occur secondarily as a result of decreased portal reflow, with eventual graft failure. Therefore, monitoring serum hyaluronic acid for the assessment of SEC function, and hepatic venous oxygen saturation levels for evaluation of hepatic microcirculation after reperfusion might be useful to estimate the prognosis of a graft after liver transplantation.2.In our second study, we examined whether insertion of an antisense vector into the allograft could down-regulate the expression of the target antigens and to prevent the rejection of transplanted organs. In vitro study, down-regulation of donor MHC class I antigen expression on the donor cells was observed after transfection of plasmid vector containing antisense of donor target antigen in vitro and also immunological response to these cells. However, in vivo, efficient transfection of antisense DNA to the donor graft organ was very difficult at present. Now we are developing new technology to provide for efficient in vivo transfection.