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Secretin Treatment Promotes Hepatic Progenitor Cell Activation, Ductal‐Canalicular Junction Formation and Amelioration of Liver Damage in a Model of Late‐Stage Primary Biliary Cholangitis

PBC is a cholestatic disease characterized by bile duct loss, ductular reaction and liver fibrosis. The canals of Hering (CoH) are the site of ductulo‐canalicular junction (DCJ) that maintain proper bile drainage from the liver, and contain the hepatic progenitor cell (HPC) population. CoH loss is noted in PBC and correlates with scoring. Secretin binds to its receptor (SR, expressed by large cholangiocytes) to promote biliary proliferation during cholestasis; however, during large duct damage, small cholangiocytes acquire large cholangiocyte phenotypes including SR expression. Secretin/SR expression is downregulated in late‐stage PBC; therefore, we aimed to understand the role of the secretin/SR axis during PBC. We hypothesized that secretin treatment restores DCJ through HPC activation and ameliorates liver phenotypes associated with late‐stage PBC.