Cyclin D1 is required for proliferation of Olig2-expressing progenitor cells in the injured cerebral cortex

Nobs, Lionel and Nestel, Sigrun and Kulik, Akos and Nitsch, Cordula and Atanasoski, Suzana. (2013) Cyclin D1 is required for proliferation of Olig2-expressing progenitor cells in the injured cerebral cortex. Glia, 61 (9). pp. 1443-1455.

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Little is known about the molecular mechanisms driving proliferation of glial cells after an insult to the central nervous system (CNS). To test the hypothesis that the G1 regulator cyclin D1 is critical for injury-induced cell division of glial cells, we applied an injury model that causes brain damage within a well-defined region. For this, we injected the neurotoxin ibotenic acid into the prefrontal cortex of adult mice, which leads to a local nerve cell loss but does not affect the survival of glial cells. Here, we show that cyclin D1 immunoreativity increases drastically after neurotoxin injection. We find that the cyclin D1-immunopositive (cyclin D1+) cell population within the lesioned area consists to a large extent of Olig2+ oligodendrocyte progenitor cells. Analysis of cyclin D1-deficient mice demonstrates that the proliferation rate of Olig2+ cells diminishes upon loss of cyclin D1. Further, we show that cyclin-dependent kinase (cdk) 4, but not cdk6 or cdk2, is essential for driving cell division of Olig2-expressing cells in our injury model. These data suggest that distinct cell cycle proteins regulate proliferation of Olig2+ progenitor cells following a CNS insult.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Former Units at DBM > Cellular Neurobiology (Atanasoski)
UniBasel Contributors:Atanasoski, Suzana and Nobs, Lionel and Nitsch, Cordula
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Wiley Liss
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:30 Aug 2018 15:12
Deposited On:31 Jan 2014 09:50

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