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Cell cycle control of Schwann cell proliferation: role of cyclin-dependent kinase-2

R Tikoo1, G Zanazzi, D Shiffman

  • 1Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|June 14, 2000
PubMed

Insights

Cyclin-dependent kinase-2 (CDK2) levels decrease during Schwann cell growth arrest. This regulation occurs transcriptionally, involving Sp1 binding sites, and suggests CDK2 is a key target for controlling Schwann cell proliferation.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Schwann cell proliferation is influenced by growth factors and axonal signals.
  • The molecular mechanisms governing Schwann cell growth arrest are not fully understood.

Purpose of the Study:

  • To investigate the regulation of cyclin-dependent kinase-2 (CDK2) in controlling Schwann cell proliferation and growth arrest.
  • To identify the molecular players involved in CDK2-mediated cell cycle regulation in Schwann cells.

Main Methods:

  • Schwann cells were cultured under various conditions (serum, forskolin, serum-free, high density).
  • Levels of CDK2 protein and mRNA were measured.
  • CDK2 promoter activity and Sp1 DNA binding were analyzed.

Main Results:

  • CDK2 protein levels were high in proliferating cells and decreased during growth arrest.
  • The decline in CDK2 was associated with reduced CDK2 mRNA and promoter activity.
  • Sp1 DNA binding sites on the CDK2 promoter were crucial for its activation in Schwann cells.

Conclusions:

  • CDK2 is a significant target for developmental signals regulating Schwann cell proliferation.
  • Regulation of CDK2 expression, partly via Sp1 transcriptional activity, plays a key role in Schwann cell growth arrest.

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