Liver X receptor α (LXRα/NR1H3) regulates differentiation of hepatocyte-like cells via reciprocal regulation of HNF4α

J Hepatol. 2014 Dec;61(6):1276-86. doi: 10.1016/j.jhep.2014.07.025. Epub 2014 Jul 27.

Abstract

Background & aims: Hepatocyte-like cells, differentiated from different stem cell sources, are considered to have a range of possible therapeutic applications, including drug discovery, metabolic disease modelling, and cell transplantation. However, little is known about how stem cells differentiate into mature and functional hepatocytes.

Methods: Using transcriptomic screening, a transcription factor, liver X receptor α (NR1H3), was identified as increased during HepaRG cell hepatogenesis; this protein was also upregulated during embryonic stem cell and induced pluripotent stem cell differentiation.

Results: Overexpressing NR1H3 in human HepaRG cells promoted hepatic maturation; the hepatocyte-like cells exhibited various functions associated with mature hepatocytes, including cytochrome P450 (CYP) enzyme activity, secretion of urea and albumin, upregulation of hepatic-specific transcripts and an increase in glycogen storage. Importantly, the NR1H3-derived hepatocyte-like cells were able to rescue lethal fulminant hepatic failure using a non-obese diabetic/severe combined immunodeficient mouse model.

Conclusions: In this study, we found that NR1H3 accelerates hepatic differentiation through an HNF4α-dependent reciprocal network. This contributes to hepatogenesis and is therapeutically beneficial to liver disease.

Keywords: HNF4A; HepaRG progenitor cell; Hepatogenesis; LXRα/NR1H3.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carbon Tetrachloride / adverse effects
  • Cell Differentiation / physiology*
  • Cell Line
  • Cell Transplantation
  • Disease Models, Animal
  • Hepatocyte Nuclear Factor 4 / physiology*
  • Hepatocytes / cytology
  • Hepatocytes / physiology*
  • Humans
  • In Vitro Techniques
  • Liver Failure / chemically induced
  • Liver Failure / therapy
  • Liver Regeneration / physiology
  • Liver X Receptors
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • Orphan Nuclear Receptors / physiology*
  • Stem Cells / cytology
  • Stem Cells / physiology*

Substances

  • HNF4A protein, human
  • Hepatocyte Nuclear Factor 4
  • Liver X Receptors
  • NR1H3 protein, human
  • Nr1h3 protein, mouse
  • Orphan Nuclear Receptors
  • Carbon Tetrachloride