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Differentiation of Embryonic Stem Cells into Oligodendrocyte Precursors
08:11

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Published on: May 19, 2010

Distinct roles for PI3K in proliferation and survival of oligodendrocyte progenitor cells

S Ebner1, M Dunbar, R D McKinnon

  • 1Departments of Surgery (Neurosurgery), Molecular Genetics, and Microbiology, UMDNJ-Robert Wood Johnson Medical School, Piscataway, New Jersey 08854, USA.

Journal of Neuroscience Research
|October 31, 2000
PubMed

Insights

Platelet-derived growth factor activates phosphoinositol 3-kinase (PI3K)-Akt signaling, independently regulating glial progenitor cell proliferation and survival. Different PI3K forms are used by early progenitors and later-maturation cells.

Area of Science:

  • Cell Biology
  • Neuroscience
  • Molecular Biology

Background:

  • Phosphoinositol 3-kinase (PI3K) signaling is crucial for cell growth and survival.
  • PI3K activates protein kinase B (Akt), a key regulator of cellular responses.
  • Oligodendrocyte progenitor cells rely on ligand-dependent signaling for proliferation, survival, and differentiation.

Purpose of the Study:

  • To investigate the role of PI3K-Akt signaling in primary oligodendrocyte progenitor cells.
  • To determine how PI3K-Akt signaling regulates proliferation, survival, and differentiation.
  • To identify specific PI3K forms involved in different progenitor cell stages.

Main Methods:

  • Primary glial (oligodendrocyte) progenitor cell culture.
  • Stimulation with platelet-derived growth factor (PDGF) and basic fibroblast growth factor-2 (FGF2).
  • Assessment of PI3K and Akt activation (Ser-473 phosphorylation) and sensitivity to wortmannin.

Main Results:

  • PI3K and Akt were activated by PDGF but not FGF2.
  • Distinct PI3K forms were activated in early progenitors versus pro-oligodendroblasts.
  • PI3K signaling was essential for both proliferation and survival of early progenitors.

Conclusions:

  • PI3K-Akt signaling independently controls proliferation and survival in oligodendrocyte progenitors.
  • The specific PI3K isoforms utilized differ between early progenitors and pro-oligodendroblasts.
  • FGF2 does not activate the PI3K pathway in these primary glial cells.

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