BACKGROUND AND AIM: Iron deposition in the liver is a common finding in patients with chronic hepatitis C (CH-C). The mechanism of this hepatic accumulation of iron is not completely understood. This study assessed if the protein expression of transferrin receptor 2 (TfR2) is upregulated in the liver of patients with CH-C and if TfR2 protein mediates iron accumulation during hepatitis C virus (HCV) infection. METHOD: Liver specimens from patients with CH-C that underwent interferon (IFN) therapy (n=23) and from patients with CH-B (n=18) were evaluated. Hepatic expression of TfR2 protein was analyzed by immunohistochemistry. Total hepatic iron score (THIS) was evaluated by Prussian blue staining. RESULTS: TfR2 protein was expressed in the cell membrane and cytosol of hepatocytes. Cytosol TfR2 protein was found to co-localize with Tf. THIS (P=0.0198) and hepatic TfR2 (P=0.0047) expression were significantly higher in CH-C than in CH-B. The change in THIS values (rho=0.580, P=0.0079) and the grade of histological activity (rho=0.444, P=0.0373) were significantly correlated with changes in TfR2 expression after IFN therapy. CONCLUSIONS: The protein expression of TfR2 is significantly associated with iron deposition in the liver in patients with CH-C. HCV infection may affect the hepatic expression of TfR2, leading to iron accumulation in the liver.
Role of transferrin receptor 2 in hepatic accumulation of iron in patients with chronic hepatitis C
MALAVASI, Fabio;
2006-01-01
Abstract
BACKGROUND AND AIM: Iron deposition in the liver is a common finding in patients with chronic hepatitis C (CH-C). The mechanism of this hepatic accumulation of iron is not completely understood. This study assessed if the protein expression of transferrin receptor 2 (TfR2) is upregulated in the liver of patients with CH-C and if TfR2 protein mediates iron accumulation during hepatitis C virus (HCV) infection. METHOD: Liver specimens from patients with CH-C that underwent interferon (IFN) therapy (n=23) and from patients with CH-B (n=18) were evaluated. Hepatic expression of TfR2 protein was analyzed by immunohistochemistry. Total hepatic iron score (THIS) was evaluated by Prussian blue staining. RESULTS: TfR2 protein was expressed in the cell membrane and cytosol of hepatocytes. Cytosol TfR2 protein was found to co-localize with Tf. THIS (P=0.0198) and hepatic TfR2 (P=0.0047) expression were significantly higher in CH-C than in CH-B. The change in THIS values (rho=0.580, P=0.0079) and the grade of histological activity (rho=0.444, P=0.0373) were significantly correlated with changes in TfR2 expression after IFN therapy. CONCLUSIONS: The protein expression of TfR2 is significantly associated with iron deposition in the liver in patients with CH-C. HCV infection may affect the hepatic expression of TfR2, leading to iron accumulation in the liver.
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