For acquiring such imaging in a mouse liver, we developed a metallic liver window device to fix a liver that is affected by movement caused by heartbeats.
The above experiments indicated that IGF2 expression showed significant discrimination ability for mouse liver tumors developed in cirrhotic and non-cirrhotic backgrounds.
Interestingly, TIMP1 activity regulates COL1 deposition in the skin (Yokose et al., 2012) and transgenic mice overexpressing PDGFC in the liver develop fibrosis with increased COL1 content (Lai et al., 2011), whereas PDGFC and PDGFRα knockout mice develop skin blistering (Soriano, 1997; Tallquist and Soriano, 2003).
When implanted into mouse liver, these cells developed into HCC's that showed recurrent amplification of the chromosomal locus harbouring Yap.
To investigate mesenchymal-epithelial transition in liver development, we analyzed the phenotype of cells and MET molecules in developing and adult mouse livers (Figure 1).
HCC that developed in PBP/MED1ΔLiv mouse livers were transplantable in athymic nude mice and these maintained PBP/MED1fl/fl genotype.
A relatively low capacity to maintain normal methylation status appears to explain, in part, the high propensity of the B6C3F1 mouse to develop liver tumors.
Of note is that although the absence of FXR/ Fxr inhibits liver growth, Fxr-KO mice spontaneously develop liver tumors as they age, asserting that BA-induced DNA damage in Fxr-KO mice may be critical in liver tumor development even if FXR/ Fxr absence limits liver regeneration.
To address these questions, we investigated the mesenchymal characteristics of fetal liver cells and observed MET in developing mouse liver.
After confirming that MET occurs in the developing mouse liver, we attempted to uncover the relationship between MET and hepatic stem cells, which are related to liver development.
