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Metzincins, including matrix metalloproteinases and meprin, in kidney transplantation Berthier C; Marti HPSwiss Med Wkly 2006[Dec]; 136 (49-50): 789-94Chronic allograft nephropathy, including chronic rejection, remains one of the major causes of renal allograft failure. Amongst other mediators, metzincins, such as matrix metalloproteinases (MMP), direct extracellular matrix metabolism and cell proliferation. Thus, we hypothesized, that these proteolytic enzymes are differentially regulated in chronic renal transplant rejection in rats and in human renal allograft nephropathy. Our studies demonstrated on the experimental level and in humans an overall up-regulation of MMP, tissue inhibitors of metalloproteinases (TIMP) and related enzymes as a result of rejection processes. Thus, metzincins may represent novel markers and therapeutic targets with respect to renal allograft rejection.|Animals[MESH]|Cyclosporine/pharmacology/therapeutic use[MESH]|Disease Models, Animal[MESH]|Extracellular Matrix Proteins/genetics/metabolism[MESH]|Graft Rejection/drug therapy/*metabolism[MESH]|Humans[MESH]|Kidney Transplantation/*physiology[MESH]|Matrix Metalloproteinases/drug effects/genetics/*metabolism[MESH]|Oligonucleotide Array Sequence Analysis[MESH]|RNA, Messenger/metabolism[MESH]|Rats[MESH]|Tiopronin/metabolism[MESH]|Tissue Inhibitor of Metalloproteinase-2/genetics/*metabolism[MESH]|Transplantation, Homologous[MESH]|Up-Regulation[MESH] |
