The demethylation of the MMP-9 gene promoter region may be involved in the occurrence and development of diabetic nephropathy by regulating the expression of MMP-9 protein in serum.
Overall, our results suggested that miR-21 may contribute to the pathogenesis of cardiac fibrosis with DN by target MMP-9, and that miR-21 may be a new possible therapeutic target for ARB in cardiac fibrosis with DN.
Treatment of DN rats with PTY-2 significantly attenuated the severity of DN by increasing the expression and activity of Mmp-9, consequently degrading the ECM accumulated in kidney tissue.
<b>Methods:</b> MMP2 and MMP9 expression was detected by immunohistochemistry in sections from renal biopsy specimens with class III, class IV and class V LN (total <i>n</i> = 31), crescentic immunoglobulin A nephropathy (<i>n</i> = 6), pauci-immune glomerulonephritis (<i>n</i> = 7), minimal change disease (<i>n</i> = 2), mesangiocapillary glomerulonephritis (<i>n</i> = 7), diabetic nephropathy (<i>n</i> = 12) and histologically normal controls (<i>n</i> = 8).
Here we used an MMP-9 gene knockout mouse model, with in vitro experiments and clinical samples, to determine the possible role of MMP-9 in diabetic nephropathy.
The urinary mRNA levels of α-SMA, fibronectin and MMP-9 were significantly higher in the DN group compared with controls (P < 0·05), and mRNA levels increased with DN progression.
Our objective was to determine whether NGAL/MMP-9 dysregulation might contribute to or serve as a biomarker of diabetic nephropathy in type 1 DM (T1DM).
However, genotyping of alleles at the MMP9 promoter microsatellite locus D20S838 in individual genomic DNA samples supported previous evidence of association between this locus and diabetic nephropathy.
Zymography, Western blotting, and immunofluorometric analysis of DNP urine showed a significant association especially between activation of MMP-9 as well as PMN-type MMP-8 and TRY-2.
We found that thrombospondin 1 (THBS1) and cyclooxygenase 1(COX1) genes were over-expressed in patients with diabetic nephropathy, and matrix metalloproteinase 9 (MMP9) and cyclooxygenase 2 (COX2) genes had lower expression in diabetic nephropathy.
To identify the genetic marker for diabetic nephropathy, we examined the association between the (A-C)n dinucleotide repeat polymorphism upstream of the matrix metalloproteinase-9 (MMP-9) gene and diabetic nephropathy in a group of Japanese patients with type 2 diabetes.