Ductular reaction cells display an inflammatory profile and recruit neutrophils in alcoholic hepatitis

Plasticity of adult hepatocytes and readjustment of cell fate: a novel dogma in liver disease

“…In addition, these cells express IGF2BP3-, phospho-mothers against decantaplegic homologue (pSMAD2), SRY-Box9 (SOX9) and pan-cytokeratin (CK) positive—fetal markers—indicating that YAP activation may alter the fate of about 75% of adult hepatocytes which develop into progenitor cells. A further support of these data is found in a recent study7 where expansion of HPCs correlated with extensive liver damage and high patient mortality, indicating that HPCs proliferation might be detrimental to a correct liver function. Nevertheless, altogether these observations in patients with ALF warrant future studies using both a bigger cohort and a greater spectrum of liver disease.…”

β-Catenin-NF-κB-CFTR interactions in cholangiocytes regulate inflammation and fibrosis during ductular reaction

“…Its role as a source of de novo hepatocytes through the process of transdifferentiation is indisputable in preclinical models shown by many fate-tracing studies 14,21,32,34 . At the same time, DR can induce fibrosis by secreting pro-inflammatory and profibrogenic factors to contribute to the disease process 7,8,9,29,35 . What drives the pro-inflammatory and pro-fibrogenic phenotype of these reactive BECs and what reverts these cells back to normal, is poorly understood.…”

Wnt/β‐catenin signalling controls bile duct regeneration by regulating differentiation of ductular reaction cells

“…8 Related studies have shown that DRCs are a cell group different from liver progenitor cells (HPCs) and have their unique repair function. 36 An essential prerequisite for biliary repair is that DRCs can reconstruct the biliary structure. 37 In this study, In DR studies, EpCAM and SOX9 are often identified as stem cell markers.…”