Hepatic progenitor cells in human liver diseases
Section snippets
Hepatic progenitor cells in human liver: localization, phenotype and comparison to animal liver
Hepatic progenitor cells (HPCs) are small epithelial cells with an oval nucleus and scant cytoplasm. They were firstly described in rat liver and the shape of their nucleus inspired Farber1 to coin them ‘oval cells’. This name has since then consistently been used for HPCs in animal liver. It has been shown in both animal and human liver that HPCs are bipotential cells that can differentiate towards the biliary and the hepatocytic lineage.2., 3., 4., 5., 6., 7., 8. Differentiation towards
Activation of human hepatic progenitor cells
‘Activation’ of HPCs or oval cells is a term which is used to refer to an increase in the number of HPCs and differentiation of the HPCs towards the biliary and/or hepatocytic lineage.23., 24. HPC activation only takes place when damage and loss of hepatocytes and/or cholangiocytes is combined with impaired regeneration of the mature cell type involved.25 Since almost all human liver diseases are characterized by a certain degree of damage, loss and impaired regeneration of hepatocytes and/or
The role of hepatic progenitor cells in tumor development in animal and human liver
It has been thought for a long time that the mature hepatocyte represents the cell of origin of all hepatocellular carcinomas (HCCs). The results of several studies performed in recent years indicate that this concept is not correct. In a number of animal models of hepatocarcinogenesis, the development of HCC is preceded by oval cell activation and the HCCs in these animal models express oval cell marker such as OV-6 and alpha-fetoprotein.39., 57., 58., 59. This indicates that oval cells
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Cited by (179)
Specific knockdown of Y-box binding protein 1 in hepatic progenitor cells inhibits proliferation and alleviates liver fibrosis
2022, European Journal of PharmacologyCitation Excerpt :It is unclear why collagen deposition occurs in the portal areas, whereas damage occurs in the lobular sites. Recent studies suggested that DR caused by the expansion of HPCs plays an important role in periportal fibrosis, although it remains controversial whether DR causes collagen deposition or collagen deposition causes DR (Glaser et al., 2009; Libbrecht and Roskams, 2002; Sato et al., 2019). In clinical research, Gadd et al. (2014) found that HPC proliferation is related to the degree of the inflammatory response and indirectly promoted the development of fibrosis in 33 patients with NAFLD (Gadd et al., 2014).
Hepatic Stem/Progenitor Cell Activation Differs between Primary Sclerosing and Primary Biliary Cholangitis
2018, American Journal of PathologyHepatic Progenitor Cells: An Update
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