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Study on the Activity of PI3K/AKT, Death Receptor and 14-3-3 Mediated Signaling Pathways Regulating Hepatocyte Apoptosis during Rat Liver Regeneration

Author

Listed:
  • X.Q. Guo
  • M.H. Li
  • T.T. Xu
  • C.F. Chang
  • G.P. Wang
  • C.S. Xu

Abstract

Studies have shown that apoptosis is closely related to the rat liver regeneration. To understand the mechanism of hepatocyte apoptosis during rat liver regeneration at the gene transcription level, the Rat Genome 230 2.0 Array was used to determine the expression changes of genes. Then the genes associated with cell apoptosis were searched by GO and NCBI databases, and cell apoptosis signaling pathways were searched by the database of QIAGEN and KEGG. Their signaling activities were calculated by spectral function E(t). The mechanism of hepatocyte apoptosis during rat liver regeneration was analyzed by Ingenuity Pathway Analysis 9.0 (IPA). The results showed that among the 27 signaling pathways regulating cell apoptosis, the E(t) values of Apoptosis signaling pathway and 14-3-3 mediated signaling pathway were significantly increased in the progression phase (6-72h after PH) of rat liver regeneration, and the E(t) values of hepatocyte apoptosis mediated by mitochondria rout were also significantly increased. The E(t) values of death receptor signaling pathway and PI3K/AKT branch of 14-3-3 mediated signaling pathway were significantly increased in the progression phase and the terminal phase (72-168h after PH) of rat liver regeneration, and the E(t) values of hepatocyte apoptosis mediated by cytomembrane route and nucleus route were also significantly increased. Conclusion: PI3K/AKT, death receptor and mitochondria branch played a key role in promoting cell apoptosis during rat liver regeneration.

Suggested Citation

  • X.Q. Guo & M.H. Li & T.T. Xu & C.F. Chang & G.P. Wang & C.S. Xu, 2014. "Study on the Activity of PI3K/AKT, Death Receptor and 14-3-3 Mediated Signaling Pathways Regulating Hepatocyte Apoptosis during Rat Liver Regeneration," Journal of Life Sciences Research, Asian Online Journal Publishing Group, vol. 1(4), pages 93-101.
    • Handle: RePEc:aoj:lifscr:v:1:y:2014:i:4:p:93-101:id:610
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