basic research for ischemia reperfusion injury following lung transplantation using a mouse orthotropic lung transplant model

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Ischemia-reperfusion injury still remains main life-threatening complication following lung transplantation. It has been obscured that how warm ischemia affects on pulmonary graft injury as compared with classical cold preservation, when lungs are retrieved from non-heart beating donors. To clarify the differences between warm and cold preserved lungs in molecular mechanisms, PCR and western-blotting assays were performed to see the changes in expression levels of transcription factors, the downstream target genes, and phosphorylations of MAP kinases. We also employed Egr-1 knock out mouse to look at the effects of Egr-1 on graft functions and inflammatory gene expressions. When Egr-1 in the pulmonary grafts was deleted, lungs functioned obviously better than grafts from wild type mouse with Egr-1 expression. Up-regulation of inflammatory cytokines expression was not observed in Egr-1 KO grafts. These results suggest a novel possible approach to avoid pulmonary graft function from severe ischemia-reperfusion injury.