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Expression of MMP-2 and TIMP-1 in Renal Tissue of Patients with Chronic Active Antibody-mediated Renal Graft Rejection

Qiang Yan1, Weiguo Sui1, Baoyao Wang1, Hequn Zou2*, Guimian Zou1 and Hao Luo3

Author Affiliations

1 Dialysis and Kidney Transplantation Center of PLA, 181 Hospital of PLA, Guilin, 541002, China

2 Institute of Nephrology and Urology, Third Affiliated Hospital of Southern Medical University, Guangzhou, 510630, China

3 First Clinical College of Southern Medical University, Guangzhou, 510515, China

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Diagnostic Pathology 2012, 7:141  doi:10.1186/1746-1596-7-141

Published: 12 October 2012



To investigate the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metallopropteinase-1 (TIMP-1) in the renal allografts of patients with chronic active antibody-mediated rejection (AMR), and to explore their role in the pathogenesis of AMR.


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.

Virtual Slides

The virtual slide(s) for this article can be found here: webcite

Matrix metalloproteinase-2; Tissue inhibitor of metalloproteinase-1; Chronic active antibody-mediate rejection; Interstitial fibrosis and tubular atrophy