International Union for Circumpolar Health Ministry of Public Health and Social Development of RF Russian Academy of Medical Sciences Siberian Branch of Russian Academy of Medical Sciences Siberian Branch of Russian Academy of Sciences Medical Polar Fund “Science” The Northern Forum |
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Seminar Infection Diseases in Arctic
Matrix metalloproteases (MMPs) are involved in many pathological processes, related to degradation of components of extracellular matrix. MMP-2 expression was shown to increase during fibrogenesis (Leroy et al., 2004). Recent studies suggested that inhibition of MMP-2 activity or blockade of MMP-2 synthesis might effectively prevent cell proliferation and collagen I synthesis Metalloproteases activities are regulated by two major types of endogenous inhibitors - alpha2-macroglobulin and tissue inhibitors of metalloproteases (TIMPs), and TIMPs inhibit all MMPs (Nagase H. et al., 2006).
The aim – to evaluate tissue inhibitor of metalloproteases type 1 (TIMP-1) in serum of patients with chronic viral hepatitis C as possible index of liver cell injury and fibrosis development.
Methods used: TIMP-1 concentration was measured in serum of patients with help of human ELISA kits (Ray Biotech, USA). Star 30 reader (USA) was used (450 nm) Diagnosis of chronic hepatitis C was made on the basis of ELISA and PCR analysis and data of liver biopsy.
Results. Liver function test (ALT activity) was moderately increased in HCV group (35 patients) and patients with liver cirrhosis (21 patients). Comparatively to control serum (20 donors) there was a tendency to increase TIMP-1 concentration in serum of patients with HCV and liver cirrhosis (statistically non-significant), whereas MMP-2 concentration was increased in group of patients with HCV. The increased expression of tissue inhibitors of MMPs (mainly TIMP-1) has been demonstrated in human fibrotic liver disease and animal models of liver fibrosis (Cao et al., 2006). One can conclude that determination of MMP-2 and TIMP-1 can provide additional information on liver injury and fibrosis development in HCV and liver cirrhosis.
Note. Abstracts are published in author's edition
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