[Hepatic progenitor cell activation and expansion in human liver cirrhosis].

Objectives: To confirm whether human hepatic progenitor cells (HPCs) occur in human liver cirrhosis, to investigate the relationship between the degree of HPCs activation and the degree of liver inflammation and to provide evidence that HPCs can differentiate into hepatocytes.
Methods: Surgical specimens from 30 human cirrhotic livers and from 3 normal livers were investigated by light microscopy and immunohistochemical staining for CK7 (a marker of biliary differentiation) and SMA (a marker of hepatic stellate cell activation). The degree of portal inflammation was determined on routine stained sections. The number of HPCs and intermediate hepatocytes and the extent of the ductular reaction were assessed.
Results: HPCs and ductular reaction were not observed in the normal livers. In liver cirrhosis cases the HPCs originated from the portal areas. With the increase of portal inflammation, HPCs and ductular reaction extending from the periphery of the liver cirrhosis nodules to the liver parenchyma and the intermediate hepatocyte proliferation were observed. The notable hepatic stellate cell activation occurred around the HPCs and ductular reaction. The number of HPCs and the extent of ductular reaction increased significantly as the portal inflammation increased. There were significant correlations between the number of HPCs with the number of intermediate hepatocytes. In addition, there was a strong correlation between the ALT and AST with the number of HPCs and intermediate hepatocytes.
Conclusion: Human hepatic progenitor cell activation exists in human liver cirrhosis. The inflammation is a trigger for HPCs activation. HPCs migration from the portal area to liver parenchyma and their differentiation into hepatocytes are important pathways for liver regeneration.