Matrix metalloproteinase-9 in fulminant hepatic failure

✍ Scribed by Lluis Palenzuela; Antoni Mas; Joan Montaner; Juan Cordoba

• Publisher: John Wiley and Sons
• Year: 2010
• Tongue: English
• Weight: 304 KB
• Volume: 51
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.23558

✦ Synopsis

After reading the article by Taura et al. with great interest, we really appreciate the ingenious work they have done. 1 In this study, they found type I collagen-producing cells do not originate from hepatocytes in a triple transgenic mouse model. Hepatocytes in vivo neither express mesenchymal markers nor exhibit a morphological change. All these results strongly challenge the earlier concept that hepatocytes in vivo acquire a mesenchymal phenotype through epithelial-mesenchymal transition (EMT) to produce the extracellular matrix (ECM), leading to liver fibrosis. Although they have provided solid evidence to show that EMT does not contribute to ECM in the process of liver fibrosis, several issues need to be further discussed.

The EMT phenomenon was first clearly demonstrated by Kaimori 2 and Zeisberg 3 simultaneously in mouse liver fibrosis. Although Taura et al. challenge the concept in vivo, the three groups independently showed that isolated primary hepatocytes exhibited fibroblast-like morphological change. Therefore, the different biological behaviors of hepatocytes in liver fibrosis between in vivo and in vitro models need to be reassessed. Studies on gene expression profiles of activated hepatic stellate cells revealed the