%0 Journal Article
%T Expression of MMP-2 and TIMP-1 in Renal Tissue of Patients with Chronic Active Antibody-mediated Renal Graft Rejection
%A Qiang Yan
%A Weiguo Sui
%A Baoyao Wang
%A Hequn Zou
%A Guimian Zou
%A Hao Luo
%J Diagnostic Pathology
%D 2012
%I BioMed Central
%R 10.1186/1746-1596-7-141
%X Immunohistochemistry assay and computer-assisted image analysis were used to detect the expression of MMP-2 and TIMP-1 in the renal allografts with interstitial fibrosis and tubular atrophy (IF/TA) in 46 transplant recipients and 15 normal renal tissue specimens as the controls. The association of the expression level of either MMP-2 or TIMP-1 with the pathological grade of IF/TA in AMR was analyzed.The expression of either MMP-2 or TIMP-1 was significantly increased in the renal allografts of the recipients as compared with the normal renal tissue (P£¿<£¿0.05). MMP-2 expression tended to decrease, while TIMP-1 and serum creatinine increased along with the increase of pathological grade of IF/TA (P£¿<£¿0.05). In IF/TA groups, the expression of TIMP-1 was positively correlated to serum creatinine level (r£¿=£¿0.718, P£¿<£¿0.05).It is suggested by the results that abnormal expressions of MMP-2 and TIMP-1 might play roles in the development of renal fibrosis in chronic AMR.The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1128474926172838 webciteC4d was found to sedimentate in peritubular capillaries in renal allografts in 1993. Since then it was looked as a sensitive indicator to detect humoral rejection and was included in Banff 07 pathologic diagnostic criteria, therefore chronic active antibody-mediated rejection (AMR) was being paid more and more attention [1]. However the exact pathogenesis of that was not full elucidated. Renal fibrosis, including renal interstitial fibrosis and glomerular sclerosis, is the common pathological mechanism of various chronic kidney diseases including chronic renal allograft dysfunction (CRAD) resulted from AMR, and finally develops into end-stage renal disease (ESRD). Previous studies suggest that matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were important cytokines for extracellular matrix (ECM) synthesis and degradation, and the excess accumul
%K Matrix metalloproteinase-2
%K Tissue inhibitor of metalloproteinase-1
%K Chronic active antibody-mediate rejection
%K Interstitial fibrosis and tubular atrophy
%U http://www.diagnosticpathology.org/content/7/1/141