Revisiting Epithelial-to-Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the “Reactive” Biliary Epithelial Phenotype

Table 1

Summary of evidence in favor of or against the existence of EMT in biliary diseases.

Model	Readouts	References
Pro-EMT
Coculture of MFs and cholangiocytes	Cholangiocytes: ↑ S100A4, ↑ Fibronectin, ↑ N-cadherin, and increased motility	[7]
Cultured cholangiocytes from α-fetoprotein (Alfp)-Cre × Rosa26-YFP mice treated with TGF, or TNF	↑ -SMA, loss of cell-cell contacts, cellular reshaping, and E-cadherin delocalization	[8]
Cultured cholangiocytes from Pkhd1^del4/del4 mouse	↑ motility due to -catenin activation	[9]
BDL rat	Coexpression of S100A4 and vimentin with K7	[7]
BDL rat	DRC (immunohistochemistry): ↑ S100A4, ↑ heat-shock protein 47, ↑ -SMA, ↓ K7, ↓ K19, and ↓ Aquaporin-1	[10]
Against-EMT
K19-CreERT × Rosa26-YFP mice, BDL	No coexpression of K19 YFP with -SMA, Desmin, or S100A4	[11]
S100A4-CreERT × Rosa26-YFP mice, BDL	No coexpression of S100A4-GFP with Pan-K cells	[11]
α-fetoprotein (Alfp)-Cre × Rosa26-YFP mice, BDL	No coexpression of YFP with S100A4, vimentin, -SMA, procollagen 12, or desmin	[8]
α-fetoprotein (Alfp)-Cre × Rosa26-YFP mice, DDC	No coexpression of YFP with S100A4, vimentin, -SMA, procollagen 12, or desmin	[8]
Human EGI-1-EGFP xenograft in SCID mice	No K19/-SMA coexpression; no expression of Y human chromosome on α-SMA^+ cells	[12]