Differentiation of neonatal rat epithelial cells from biliary origin into immature hepatic cells by sequential exposure to hepatogenic cytokines and growth factors reflecting liver development

Toxicol In Vitro. 2007 Oct;21(7):1325-31. doi: 10.1016/j.tiv.2007.03.013. Epub 2007 Apr 4.

Abstract

It was investigated whether cryopreserved rat liver epithelial cells (RLEC) from biliary origin are capable of undergoing hepatic differentiation upon sequential exposure to liver-specific factors (fibroblast growth factor (FGF)-4, hepatocyte growth factor (HGF), insulin-transferrin-sodium-selenite (ITS), dexamethasone (Dex) and oncostatin M (OSM)), reflecting liver embryogenesis in vivo. As differentiation progressed, cells acquired a hepatic morphology (polygonal-to-cuboidal shaped, binucleated cells), corresponding well with the phenotypic changes observed. Biliary cytokeratin (CK)19 and connexin (Cx)43-expression both gradually decreased; CK19-expression disappeared even completely. In contrast, hepatic CK18-expression persisted throughout the culture time. Hepatocyte nuclear factor (HNF)3beta, alpha-foetoprotein (AFP), transthyretin (TTR), HNF4, albumin (ALB), HNF1alpha, multidrug resistance protein (MRP)2 and Cx32 were expressed at specific stages during RLEC-differentiation, thereby showing a progressive hepatic maturation. Indeed, immature AFP and mature ALB were sequentially expressed, in line with the in vivo liver embryogenesis. Expression of the early and mid-late 'liver-enriched' transcription factors (LETF) HNF3beta and HNF4 declined and translocated to the cytosol, respectively, while the late LETF HNF1alpha underwent a nuclear upregulation. In conclusion, RLEC are bipotent cells, capable of differentiation into immature hepatocytes in a hepatic-stimulating micro-environment. The robustness of the sequential conditions, developed before for hepatic 'transdifferentiation' of rat bone marrow stem cells (rBMSC), was hereby confirmed.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cell Differentiation / drug effects*
  • Cell Differentiation / physiology
  • Connexin 43 / genetics
  • Connexin 43 / metabolism
  • Cryopreservation
  • Cytokines / pharmacology*
  • Dexamethasone / pharmacology
  • Epithelial Cells
  • Fibroblast Growth Factor 4 / pharmacology
  • Gene Expression Regulation*
  • Hepatocyte Growth Factor / pharmacology
  • Hepatocytes / metabolism*
  • Insulin / pharmacology
  • Keratin-19 / genetics
  • Keratin-19 / metabolism
  • Oncostatin M / pharmacology
  • Phenotype
  • Rats
  • Sodium Selenite / pharmacology
  • Time Factors
  • Transferrin / pharmacology

Substances

  • Connexin 43
  • Cytokines
  • Fibroblast Growth Factor 4
  • Insulin
  • Keratin-19
  • Transferrin
  • Oncostatin M
  • Hepatocyte Growth Factor
  • Dexamethasone
  • Sodium Selenite