STAT3 Down-regulates the Expression of Cyclin D during Liver Development

We show that the expression of D-type cyclins including cyclin D1, D2, and D3 is down-regulated along with liver development

Takaaki Matsui; Taisei Kinoshita; Toshio Hirano; Takashi Yokota; Atsushi Miyajima

2002

Scholarcy highlights

  • The cell cycle is tightly regulated by cell cycle regulatory molecules including cyclins, cyclin-dependent kinases,1 and CDK inhibitors
  • By using a primary culture of fetal hepatocytes derived from murine embryos at embryonic day 14.5, it was demonstrated that STAT3 and K-Ras mediate the oncostatin M signaling for functional maturation of fetal hepatocytes into neonatal liver cells and morphological changes including the formation of E-cadherin-based adherens junctions, respectively
  • Developmental Regulation of the Expression of D-type Cyclins in the Liver—As the expression of cyclin D1 is rapidly induced during liver injury, it is believed that D1 cyclin plays an essential role in the proliferation of hepatocytes during liver regeneration
  • Fetal hepatocytes first appear at E8.5 and proceed through a series of maturation steps including autonomous proliferation, cellular enlargement, tight cell-cell contacts, growth arrest, and functional maturation
  • Expression of cyclin D3 was down-regulated during liver development in vivo, OSM failed to down-regulate the expression of D3 cyclin in fetal hepatocytes in vitro
  • The result that OSM failed to down-regulate D3 cyclin suggests that D3 expression is regulated by signals other than those induced by OSM and that down-regulation of D3 expression is not required for the expression of various genes and functions in neonatal liver
  • These findings again suggest that the cyclin D1 gene is an important target of STAT3 in hepatocytes and that its regulation by STAT3 varies dependent on the cell stage, i.e. proliferation or differentiation

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