OBJECTIVE: To explore the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the renal tissue of patients with IgA nephropathy. METHODS: Immunohistochemistry and in situ hybridization assays were applied to detect the expression of mRNA and protein of TIMP-1, as well as the protein expression of MMP-9 in renal tissue of 38 patients with IgA nephropathy. RESULTS: MMP-9 was normally expressed, at a low level, in the glomerular endothelial cells and visceral epithelial cells, as well as in tubular epithelial cells and walls of vessels. The expression of MMP-9 was significantly increased in mesangial proliferative glomeruli and interstitial vascular walls of IgA nephropathy patients (P < 0.001), but markedly decreased in sclerotic glomeruli and not apparently altered in the tubule. No expression of TIMP-1 could be detected in normal renal tissue. TIMP-1 was only slightly expressed in the mesangioproliferative glomeruli of IgA nephropathy patients. TIMP-1 expression was increased notably in partially sclerotic glomeruli, and most prominently expressed in tubulointerstitium (P < 0.01), mainly in tubular epithelial cells, interstitial cells, and vascular endothelial cells. The expression of TIMP-1 was distinctly associated with the level of serum creatinine (P < 0.05), tubulointerstitial fibrosis (P < 0.01), and tubulointerstitial infiltration of leukocytes (P < 0.01). MMP-9 expression did not correlate with proteinuria, but negatively correlated with serum creatinine levels (P < 0.05). CONCLUSION: The abnormal expressions of MMP-9 and TIMP-1 may contribute to the progression of IgA nephropathy.
OBJECTIVE: To explore the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the renal tissue of patients with IgA nephropathy. METHODS: Immunohistochemistry and in situ hybridization assays were applied to detect the expression of mRNA and protein of TIMP-1, as well as the protein expression of MMP-9 in renal tissue of 38 patients with IgA nephropathy. RESULTS:MMP-9 was normally expressed, at a low level, in the glomerular endothelial cells and visceral epithelial cells, as well as in tubular epithelial cells and walls of vessels. The expression of MMP-9 was significantly increased in mesangial proliferative glomeruli and interstitial vascular walls of IgA nephropathypatients (P < 0.001), but markedly decreased in sclerotic glomeruli and not apparently altered in the tubule. No expression of TIMP-1 could be detected in normal renal tissue. TIMP-1 was only slightly expressed in the mesangioproliferative glomeruli of IgA nephropathypatients. TIMP-1 expression was increased notably in partially sclerotic glomeruli, and most prominently expressed in tubulointerstitium (P < 0.01), mainly in tubular epithelial cells, interstitial cells, and vascular endothelial cells. The expression of TIMP-1 was distinctly associated with the level of serum creatinine (P < 0.05), tubulointerstitial fibrosis (P < 0.01), and tubulointerstitial infiltration of leukocytes (P < 0.01). MMP-9 expression did not correlate with proteinuria, but negatively correlated with serum creatinine levels (P < 0.05). CONCLUSION: The abnormal expressions of MMP-9 and TIMP-1 may contribute to the progression of IgA nephropathy.