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This article is part of the supplement: 11th International Symposium on the Cells of the Hepatic Sinusoid and their Relation to Other Cells

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N-Cadherin cleavage during activated hepatic stellate cell apoptosis is inhibited by tissue inhibitor of metalloproteinase-1

Frank Murphy1*, Julian Waung1, Jane Collins2, Michael JP Arthur1, Hideaki Nagase3, Derek Mann1, R Christopher Benyon1 and John P Iredale1

Author Affiliations

1 Liver group, Division of Infection, Inflammation and Repair, Southampton University, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK

2 Mucosal Immunology, Southampton University, Tremona Road, Southampton, UK

3 The Kennedy Institute, Imperial College, 1 Aspenlea Road, London W6, UK

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Comparative Hepatology 2004, 3(Suppl 1):S8  doi:10.1186/1476-5926-2-S1-S8

Published: 14 January 2004

Abstract

Apoptosis of hepatic stellate cells (HSC) has previously been shown to occur during spontaneous resolution of experimental liver fibrosis. TIMP-1 has also been shown to have a key role because of its ability to inhibit apoptosis of HSC via matrix metalloproteinase (MMP) inhibition. This has led to further study of novel substrates for MMPs that might impact on HSC survival. N-Cadherin is known to mediate cell-cell contacts in fibroblasts. In this study we demonstrate that N-Cadherin is expressed by activated rat HSC. Furthermore, during apoptosis of HSC, the N-Cadherin is cleaved into smaller fragments. Apoptosis of HSC may be inhibited by TIMP-1. This is associated with reduced fragmentation of N-Cadherin. N-Cadherin may have an important role in supporting HSC survival while N-Cadherin cleavage may play a part in promoting HSC apoptosis in recovery from liver fibrosis.