Vps33b is crucial for structural and functional hepatocyte polarity.

ABSTRACT:

Background & aims

In the normal liver, hepatocytes form a uniquely polarised cell layer that enables movement of solutes from sinusoidal blood to canalicular bile. Whilst several cholestatic liver diseases with defects of hepatocyte polarity have been identified, the molecular mechanisms of pathogenesis are not well defined. One example is arthrogryposis, renal dysfunction and cholestasis syndrome, which in most patients is caused by VPS33B mutations. VPS33B is a protein involved in membrane trafficking that interacts with RAB11A at recycling endosomes. To understand the pathways that regulate hepatocyte polarity better, we investigated VPS33B deficiency using a novel mouse model with a liver-specific Vps33b deletion.

Methods

To assess functional polarity, plasma and bile sa

SUBMITTER: Hanley J 

PROVIDER: S-EPMC5387182 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature