Mitochondrial nitric oxide synthase drives redox signals for proliferation and quiescence in rat liver development

We examined liver Mitochondrial nitric oxide synthase modulation and mitochondrial redox changes in developing rats from embryonic days 17–19 and postnatal day 2 through postnatal days 15–90. mitochondrial nitric oxide synthases expression and activity were almost undetectable in fetal liver, and progressively increased after birth by tenfold up to adult stage

Mar�a C. Carreras

2004

Scholarcy highlights

  • We report the modulation of Mitochondrial nitric oxide synthase activity and the putative regulation of cell cycle redox signaling in the sequence of proliferating to quiescent cell stages during rat liver development
  • Transition from fetal to adult liver is accompanied by a burst of hepatocyte proliferation in late gestation and in the immediate neonatal period, followed by a decrease of proliferation after the first postnatal week
  • Mitochondria isolated from maximally proliferating liver at E19 –P2 retained 40%–50% of complex I, II-III, and IV activities of quiescent organelles; mitochondrial ubiquinone had a similar pattern
  • The present results suggest that synchronized increase of mitochondrial activities, mtNOS, andss operates on the balance of liver signaling pathways to drive the transition from proliferation to quiescence
  • We recently reported that a critical reduction of mtNOS activity andss contribute to tumoral persistent behavior
  • We recently reported that a critical reduction of Mitochondrial nitric oxide synthase activity andss contribute to tumoral persistent behavior. Further studies could confirm the contribution of mitochondrial redox signaling to the modulation of cyclins D2 and D3, which parallels cyclin D1 expression at developmental redox conditions and may play a central role in liver development

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