Intrahepatic expression of the hepatic stellate cell marker fibroblast activation protein correlates with the degree of fibrosis in hepatitis C virus infection

Background: Activated hepatic stellate cells (HSCs), recognised by their alpha smooth muscle actin immunoreactivity, are primarily responsible for liver fibrosis. However, the presence of alpha smooth muscle actin positive HSCs is not always associated with the development of liver fibrosis. Recently, other markers of human HSCs including the gelatinase fibroblast activation protein (FA-P) and glial fibrillary acidic protein have been identified. Aims: We examined the relationship between the expression of these HSC markers and the severity of liver injury in patients with chronic hepatitis C virus infection. Methods: Liver tissue from 27 patients was examined using immunohistochemistry. Linear correlation analysis was used to compare staining scores with the stage and grade of liver injury. Results-Conclusions: FAT expression, seen at the tissue-remodelling interface, was strongly and significantly correlated with the severity of liver fibrosis. A weaker correlation was seen between glial fibrillary acidic protein expression and fibrosis stage. This contrasted with the absence of a relationship between alpha smooth muscle actin and the fibrotic score. A correlation was also observed between FAT expression and necroinflammatory score. In summary, FA-P expression identifies a HSC subpopulation at the tissue-remodelling interface that is related to the severity of liver fibrosis.