Notch-2-cKO mice treated with DDC or ANIT accumulated hepatic progenitor cells that failed to progress into mature ducts.

Proliferation assay-3H thymidine incorporation was used to detect the effect of growth factors on proliferation of hepatic progenitor cell.

The following experiments investigated the impact of TGF-beta1 on a previously described population of hepatic progenitor cells (HPC).

Adult hepatic progenitor cells are activated during regeneration when hepatocytes and bile duct epithelium are damaged or unable to proliferate.

In RBP-Jk-cKO mice, mature ducts and hepatic progenitor cells were both significantly reduced with respect to similarly treated wild type mice.

Background and aim: Liver regeneration after severe liver damage depends in part on proliferation and differentiation of hepatic progenitor cells (HPCs).

Results: In DDC treated wild type mice, pharmacologic Notch inhibition with dibenzazepine decreased the number of both ductular reaction and hepatic progenitor cells.

In normal liver, the protein is undetectable in normal mature hepatocytes and found only in some ductular cells, representing potential hepatic progenitor cells.

Here we report the identification of genes whose expression is directly regulated by FGFR activity during the transition from endoderm to hepatic progenitor cell.

At later stages, from 30 h posthepatectomy onwards, CHox-cad activity is detected predominantly in cells of the hepatic progenitor cell compartment, the portal spaces.

Extraordinary progress has been made in the field of hepatic progenitors and iPS.

These findings suggest an important attribute of EGF on opposing and reversing TGF-β1 effects, indicating the plasticity of hepatic progenitors.

Hepatic progenitor cells and stellate cells play a significant role in the development and progression of fibrosis in chronic HCV.

When this regeneration ability is impaired during liver injury, oval cells, which are considered to be postnatal hepatic progenitors, proliferate and differentiate into hepatocytes.