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Cdk2 loss accelerates precursor differentiation and remyelination in the adult central nervous system

Céline Caillava1, Renaud Vandenbosch, Beata Jablonska

  • 1UMR-S975, Centre de Recherche de l'Institut du Cerveau et de la Moelle Epinière, Université Pierre et Marie Curie-Paris 6, Paris 75013, France.

The Journal of Cell Biology
|April 20, 2011
PubMed

Insights

Cyclin-dependent kinase 2 (Cdk2) is not essential for myelin development but is crucial for adult oligodendrocyte progenitor cell renewal. Loss of Cdk2 accelerates central nervous system remyelination after demyelination.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • The role of intrinsic regulators in oligodendrocyte progenitor cell (OPC) division is not well understood.
  • Type 2 cyclin-dependent kinase (Cdk2) regulates OPC cell cycle progression, but its function in myelination and demyelinating lesion repair is unknown.

Purpose of the Study:

  • To investigate the function of Cdk2 in OPC proliferation and differentiation during central nervous system (CNS) development and in pathological conditions using a Cdk2 knockout mouse model.

Main Methods:

  • Utilized a viable Cdk2(-/-) mutant mouse model.
  • Assessed OPC cell cycle, proliferation, differentiation, and myelination in both normal development and following induced CNS demyelination.

Main Results:

  • Cdk2 deficiency did not impact OPC cell cycle, oligodendrocyte numbers, or myelination during CNS development.
  • In response to demyelination, Cdk2 loss altered adult OPC renewal, cell cycle exit, and differentiation.
  • Loss of Cdk2 significantly accelerated the remyelination of demyelinated axons in the CNS.

Conclusions:

  • Cdk2 is dispensable for normal CNS myelination but plays a critical role in adult OPC renewal and differentiation.
  • Cdk2 may represent a key mechanism influencing adult progenitor differentiation for myelin regeneration.

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