The hepatocyte is a direct target for transforming-growth factor beta activation via the insulin-like growth factor II/mannose 6-phosphate receptor

J Hepatol. 2003 Feb;38(2):156-63. doi: 10.1016/s0168-8278(02)00378-1.

Abstract

Background/aims: The cation-independent mannose 6-phosphate receptor (CIMPR) is overexpressed in hepatocytes during liver regeneration and has been implicated in the maturation of latent pro-transforming growth factor beta (TGFbeta). In this study, we have: (1) kinetically characterized the changes in CIMPR expression in regenerating liver and cultured proliferating hepatocytes; and (2) assessed the contribution of hepatocyte via the CIMPR to latent pro-TGFbeta activation.

Methods: The expression of CIMPR protein and mRNA in livers collected after partial hepatectomy and hepatocyte primary cultures was analyzed by Western and Northern blotting. Activity of latent pro-TGFbeta was assessed by inhibition of [3H] methylthymidine incorporation into DNA.

Results: The expression of the CIMPR protein and/or mRNA progressively increased after 8 h in regenerating liver and 42-46 h in cultured hepatocytes, prior to the onset of DNA replication. Both mature TGFbeta and latent pro-TGFbeta inhibited epidermal growth factor-stimulated DNA synthesis in hepatocytes in a dose-dependent manner. The effect of latent pro-TGFbeta was reversed by two ligands of the CIMPR: beta-galactosidase, a mannose 6-phosphate containing protein, and a CIMPR antibody.

Conclusions: (1) The induction of the CIMPR gene during liver regeneration and hepatocyte culture occurs in mid G1 phase; and (2) the CIMPR mediates latent proTGFbeta activation and thus may act, by targeting TGFbeta to hepatocytes, as a negative regulator of hepatocyte growth.

MeSH terms

  • Animals
  • Cell Division / drug effects
  • Cell Division / physiology
  • Cells, Cultured
  • Female
  • G1 Phase / drug effects
  • G1 Phase / physiology
  • Gene Expression / drug effects
  • Gene Expression / physiology
  • Hepatocytes / cytology
  • Hepatocytes / metabolism*
  • Ligands
  • Liver Regeneration / physiology
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology
  • Protein Precursors / metabolism
  • Protein Precursors / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, IGF Type 2 / genetics*
  • Receptor, IGF Type 2 / metabolism*
  • Transforming Growth Factor beta / metabolism
  • Transforming Growth Factor beta / pharmacology*
  • Transforming Growth Factor beta1

Substances

  • Ligands
  • Peptide Fragments
  • Protein Precursors
  • Receptor, IGF Type 2
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1