Matrilysin (MMP-7) expression in renal tubular damage: Association with Wnt4

Surendran, Kameswaran; Simon, Theodore C.; Liapis, Helen; McGuire, John K.

doi:10.1111/j.1523-1755.2004.00641.x

Cited by 92 publications

(92 citation statements)

References 43 publications

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“…A recent study demonstrated the striking down-regulation of REIC͞Dkk-3 in 15 of 17 (88%) RCC tumor samples (49). Like HGF, Wnt family members are normally expressed in kidney during development and in adulthood (19,31,50). Our results suggest that loss of this potential Wnt inhibitor combined with the frequent loss of VHL function in RCC could contribute significantly to tumorigenesis, invasion, and metastasis.…”

Section: Discussionmentioning

confidence: 77%

The von Hippel–Lindau tumor suppressor gene product represses oncogenic β-catenin signaling in renal carcinoma cells

Peruzzi

Athauda

Bottaro

2006

Proc. Natl. Acad. Sci. U.S.A.

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Section: Discussionmentioning

confidence: 77%

The von Hippel–Lindau tumor suppressor gene product represses oncogenic β-catenin signaling in renal carcinoma cells

Peruzzi

Athauda

Bottaro

2006

Proc. Natl. Acad. Sci. U.S.A.

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“…Notably, MMP-7 was the only MMP significantly upregulated in the liver of biliary atresia in these two studies. Besides the role in pulmonary fibrosis mentioned above, MMP-7 has also been found to be related to progression of tubulointerstitial fibrosis in renal tubular injury in human, 39 and to be involved in the tissue remodeling process and fibrosis of the left atria during progression of heart failure in rat. 40 Furthermore, Lichtinghagen et al 17 analyzed hepatic mRNA expression and reported that MMP-2, MMP-7, and TIMP-1 provided the best discrimination between cirrhosis and pre-cirrhotic stages in patients with chronic active hepatitis C, and steadily increasing mRNA expression with disease progression in MMP-1, -2, -7 and -14 closely correlated to the parameters of fibrogenesis in hepatitis C virus-induced liver cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Matrilysin (MMP-7) is a major matrix metalloproteinase upregulated in biliary atresia-associated liver fibrosis

et al. 2005

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Matrix metalloproteinases (MMPs) are the proteases responsible for tissue remodeling during liver fibrosis caused by various disorders including biliary atresia. However, information regarding the relative contribution of these proteases to liver fibrosis is still limited. We studied matrix metalloproteinase-2 (MMP-2), -7, -9 and -13 mRNA expressions in the liver tissue of early-stage biliary atresia at the time of Kasai's procedure, late-stage biliary atresia at the time of liver transplantation with advanced fibrosis and nondiseased control without liver fibrosis. The results of real-time quantitative reverse transcriptase-PCR analysis revealed that only MMP-2 and -7 expressions were significantly different between groups. MMP-2 was significantly higher in Liver Transplantation group than both in Control (P ¼ 0.010) and in Kasai's Procedure (P ¼ 0.001) groups, whereas the difference of MMP-2 expression between Control and Kasai's Procedure was not significant. However, the relative expression level of MMP-7 was sequentially elevated when comparing Control, Kasai's Procedure and Liver Transplantation groups, and there was significant (P ¼ 0.019) difference when comparing Control and Liver Transplantation groups. Moreover, the fold difference in MMP-7 mRNA was much higher than that in MMP-2 mRNA between groups. The expressions of MMP-7 were further confirmed by agarose gel electrophoresis and Western blotting. Immunohistochemical analysis revealed a significant positive correlation of the scores of MMP-7 immunostaining with the stages of liver fibrosis. In situ hybridization demonstrated that the bile ductular epithelial cells, Kupffer cells and hepatocytes were the major producers of matrix metalloproteinase-7 in the liver. Our results imply that MMP-7 is a major MMP associated with the tissue remodeling during the progression of liver fibrosis in biliary atresia. Modern Pathology (2005) 18, 941-950.

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“…12,13 As for the kidney, an earlier study documented an increased expression of MMP-7 in polycystic kidney disease, acute kidney injury induced by folic acid, and obstructive nephropathy. 14 However, what regulates MMP-7 expression in diseased kidneys in vivo remains enigmatic. Furthermore, little is known about the relevance of MMP-7 regulation to the progression of renal fibrotic lesions in CKDs.…”

mentioning

confidence: 99%

Matrix Metalloproteinase-7 as a Surrogate Marker Predicts Renal Wnt/β-Catenin Activity in CKD

Tan

et al. 2012

Journal of the American Society of Nephrology

133

165

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A variety of chronic kidney diseases exhibit reactivation of Wnt/b-catenin signaling. In some tissues, b-catenin transcriptionally regulates matrix metalloproteinase-7 (MMP-7), but the association between MMP-7 and Wnt/b-catenin signaling in chronic kidney disease is unknown. Here, in mouse models of both obstructive nephropathy and focal segmental glomerulosclerosis (adriamycin nephropathy), we observed upregulation of MMP-7 mRNA and protein in a time-dependent manner. The pattern and extent of MMP-7 induction were positively associated with Wnt/b-catenin signaling in these models. Activation of b-catenin through ectopic expression of Wnt1 promoted MMP-7 expression in vivo, whereas delivery of the gene encoding the endogenous Wnt antagonist Dickkopf-1 abolished its induction. Levels of MMP-7 protein detected in the urine correlated with renal Wnt/b-catenin activity. Pharmacologic blockade of Wnt/ b-catenin signaling by paricalcitol inhibited MMP-7 expression in diseased kidneys and reduced the levels detected in the urine. In vitro, b-catenin activation induced the expression and secretion of MMP-7 and promoted the binding of T cell factor to the MMP-7 promoter in kidney epithelial cells. We also observed higher levels of MMP-7 expression, which correlated with b-catenin, in kidney tissue from patients with various nephropathies. In summary, levels of renal MMP-7 correlate with Wnt/b-catenin activity, and urinary MMP-7 may be a noninvasive biomarker of this profibrotic signaling in the kidney.

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Matrilysin (MMP-7) expression in renal tubular damage: Association with Wnt4

Abstract: These observations suggest that matrilysin may have a role in renal tubular injury and progression of tubulointerstitial fibrosis, and that Wnt4 may regulate matrilysin expression in the kidney.

Cited by 92 publications

References 43 publications

The von Hippel–Lindau tumor suppressor gene product represses oncogenic β-catenin signaling in renal carcinoma cells

The von Hippel–Lindau tumor suppressor gene product represses oncogenic β-catenin signaling in renal carcinoma cells

Matrilysin (MMP-7) is a major matrix metalloproteinase upregulated in biliary atresia-associated liver fibrosis

Matrix Metalloproteinase-7 as a Surrogate Marker Predicts Renal Wnt/β-Catenin Activity in CKD

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