Rbpj deletion in hepatic progenitor cells attenuates endothelial responses and fibrosis in DDC-fed mice.

ABSTRACT:

Background

As the role of hepatic progenitor cells (HPCs) in constituting ductular reactions in pathogenesis remains ambiguous, we aimed to establish the in vivo cause-and-effect relationship between HPCs and chronic liver disease progression. We previously demonstrated that peritumoral ductules are associated with angiogenesis in liver tumors, and forkhead box L1 (Foxl1)-expressing murine HPCs secrete angiogenic factors in vitro. Therefore, we hypothesized that HPCs are capable of remodeling the portal vascular microenvironment and regulating overall liver disease progression, and this function of HPCs is dependent on recombination signal binding protein for immunoglobulin kappa J region (RBPJ), a key effector of the Notch signaling pathway.

Methods

We generated HPC-specifi

SUBMITTER: Lee S 

PROVIDER: S-EPMC12180839 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature