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(American Journal of Pathology. 2003;162:1661-1667.)
© 2003 American Society for Investigative Pathology

Identification and Characterization of the Hepatic Stellate Cell Transferrin Receptor

Kim R. Bridle*{dagger}, Darrell H.G. Crawford*{ddagger} and Grant A. Ramm*{dagger}

From the Hepatic Fibrosis Group,* The Queensland Institute of Medical Research and the Department of Medicine,{dagger} The University of Queensland; and the Departments of Gastroenterology and Hepatology,{ddagger} Princess Alexandra Hospital, Brisbane, Queensland, Australia

Activated hepatic stellate cells have been implicated in the fibrogenic process associated with iron overload, both in animal models and in human hemochromatosis. Previous studies have evaluated the role of ferritin/ferritin receptor interactions in the activation of stellate cells and subsequent fibrogenesis; however, the role of transferrin in hepatic stellate cell biology is unknown. This study was designed to identify and characterize the stellate cell transferrin receptor and to evaluate the influence of transferrin on stellate cell activation. Identification and characterization of the stellate cell transferrin receptor was determined by competitive displacement assays. The effect of transferrin on stellate cell activation was assessed using western blot analysis for {alpha}-smooth muscle actin expression, [3H]Thymidine incorporation, and real-time RT-PCR for procollagen {alpha}1(I) mRNA expression. A specific receptor for rat transferrin was observed on activated but not quiescent stellate cells. Transferrin significantly increased the expression of {alpha}-smooth muscle actin, but caused a decrease in proliferation. Transferrin induced a significant increase in procollagen {alpha}1(I) mRNA expression. In conclusion, this study has demonstrated for the first time a specific, high affinity receptor for rat transferrin on activated hepatic stellate cells, which via interaction with transferrin regulates stellate cell activation. This suggests that transferrin may be an important factor in the activation of hepatic stellate cells in conditions of iron overload.




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