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Canonical Wnt signalling is activated during BEC-to-hepatocyte conversion in vivo and modulates liver epithelial cell plasticity in hepatic organoids

Valle-Encinas, E.; Aleksieva, N.; Velasco Martinez, C.; Dawes, M.; Zverev, M.; Muller, M.; Offergeld, A.; Smalley, M. J.; Hogan, C.; Forbes, S. J.; Bird, T. G.; Dale, T. C.

2020-11-09 cell biology
10.1101/2020.11.09.374462 bioRxiv
Show abstract

While it is recognized that the Wnt/{beta}-catenin pathway orchestrates hepatocyte proliferation in both homeostasis and injury, little is known about the importance of {beta}-catenin in biliary epithelial cell (BEC) plasticity. In this study, the dynamics of activation of the canonical Wnt pathway were investigated during BEC-to-hepatocyte conversion using as a model methionine/choline deficient (MCD)-injured livers where hepatocyte proliferation was compromised by the overexpression of p21. In this model, activation of {beta}-catenin was found an event associated with BEC reprogramming. Using ductal organoids to model BECs transitioning into hepatocytes, we found that activation of the Wnt/{beta}-catenin pathway in these cells promoted partial escape from a biliary fate and triggered the acquisition of progenitor cell features. Our data furthermore support that BECs are source of Wnt ligands and that Rspo proteins potentially act as the limiting factor controlling the activation of {beta}-catenin activation and BEC reprogramming during severe liver damage.

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"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.