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Differential effects of Akt isoforms on somatic cell reprogramming.

Yong Tang1, Zongliang Jiang1, Yan Luo1

  • 1Center for Regenerative Biology, Department of Animal Science, University of Connecticut, Storrs, CT 06269, USA.

Journal of Cell Science
|July 20, 2014
PubMed
Summary

Enhanced Akt signaling, particularly Akt1 and Akt3, drives induced pluripotent stem cell (iPSC) generation by activating Stat3 and promoting cell proliferation. Inhibition of GSK3 or expression of Esrrb can rescue reprogramming when Akt is blocked.

Keywords:
AktGSK3IsoformReprogrammingStat3iPSC

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Area of Science:

  • Cell Biology
  • Stem Cell Research
  • Molecular Biology

Background:

  • The Akt signaling pathway is crucial for cell growth, proliferation, and survival.
  • The distinct roles of Akt isoforms in somatic cell reprogramming remain largely unexplored.

Purpose of the Study:

  • To investigate the specific functions of the three Akt isoforms (Akt1, Akt2, Akt3) in induced pluripotent stem cell (iPSC) generation.
  • To elucidate the molecular mechanisms by which Akt isoforms influence reprogramming efficiency and cell proliferation.

Main Methods:

  • Experimental manipulation of Akt isoform activity during iPSC generation.
  • Analysis of Stat3 activation, mTOR signaling, and LIF receptor expression.
  • Assessment of cell proliferation and reprogramming efficiency using genetic and pharmacological inhibitors (mTOR, Akt, GSK3).
  • Evaluation of the role of Esrrb in overriding Akt inhibition.

Main Results:

  • Enhanced Akt1 activity significantly promotes complete reprogramming, primarily by boosting Stat3 activation in conjunction with leukemia inhibitory factor (LIF).
  • Akt1 also facilitates colony formation and augments Stat3 activity via mTOR activation and increased LIF receptor expression.
  • Akt2 and Akt3 activation similarly enhance reprogramming and coordinate with LIF to activate Stat3.
  • Blocking Akt1 or Akt3 expression halts cell proliferation and reprogramming, while Akt2 inhibition has no such effect.
  • Inhibition of mTOR and Akt pathways, which halts proliferation and reprogramming, can be reversed by inhibiting GSK3.
  • Overexpression of Esrrb, a GSK3β target, rescues reprogramming inhibition caused by Akt pathway blockade.

Conclusions:

  • Akt signaling, particularly Akt1 and Akt3, is essential for efficient somatic cell reprogramming and subsequent cell proliferation.
  • Akt promotes pluripotency establishment through co-stimulation of Stat3 activity with LIF.
  • GSK3 inhibition and Esrrb expression can restore reprogramming under conditions of Akt pathway inhibition, highlighting their critical roles.
  • The findings reveal a complex interplay between Akt, Stat3, LIF, mTOR, GSK3, and Esrrb in regulating the reprogramming process.