title: Intrahepatic expression of the hepatic stellate cell marker fibroblast activation protein correlates with the degree of fibrosis in hepatitis C virus infection.
abstract: 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 (FAP) and glial fibrillary acidic protein have been identified.
  
  
  OBJECTIVE
  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.
  
  
  CONCLUSIONS
  FAP 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 FAP expression and necroinflammatory score. In summary, FAP expression identifies a HSC subpopulation at the tissue-remodelling interface that is related to the severity of liver fibrosis.
authors.affiliation: A.W. Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Centenary Institute of Cancer Medicine and Cell Biology and the University of Sydney, Australia. miriam-levy@hotmail.com
authors.forename: M T
authors.initials: MT
authors.lastname: Levy
authors.forename: G W
authors.initials: GW
authors.lastname: McCaughan
authors.forename: G
authors.initials: G
authors.lastname: Marinos
authors.forename: M D
authors.initials: MD
authors.lastname: Gorrell
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D000951:Antigens, Neoplasm; D015415:Biomarkers / Q000032:analysis; D014408:Biomarkers, Tumor; D017252:CD3 Complex / Q000378:metabolism; D010450:Endopeptidases; D005260:Female; D018093:Gelatinases; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006133:Growth Substances / Q000378:metabolism*; D019698:Hepatitis C, Chronic / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008103:Liver Cirrhosis / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008565:Membrane Proteins; D012697:Serine Endopeptidases / Q000378:metabolism*; D000099167:Fibroblast Activation Protein Alpha; D000097382:CD68 Molecule
chemical_list: D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000951:Antigens, Neoplasm; D015415:Biomarkers; D014408:Biomarkers, Tumor; D017252:CD3 Complex; D010450:Endopeptidases; D018093:Gelatinases; D005904:Glial Fibrillary Acidic Protein; D006133:Growth Substances; D008565:Membrane Proteins; D012697:Serine Endopeptidases; D000099167:Fibroblast Activation Protein Alpha; C067980:CD68 antigen, human; D000097382:CD68 Molecule