Cyclin D1 is required for proliferation of olig2-expressing progenitor cells in the injured cerebral cortex
10.07.2013
Nobs L, Nestel S, Kulik A, Nitsch C, Atanasoski S.
Glia. 2013;61(9):1443-55
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 cell loss but does not affect the survival of glial cells. We show that cyclin D1 staining increases after neurotoxin injection. We find that the cyclin D1-immunopositive cell population within this area consists to a large extent of Oligo2+ oligodendrocyte progenitor cells. Analysis of cyclin D1-deficient mice demonstrates that the proliferation rate of Oligo2+ cells diminishes upon loss of cyclin D1. Further, we show that cyclin-dependent kinase 4 is essentail for driving cell division of Oligo2-expressing cells in our injury model. These data suggest that distinct cell cycle proteins regulate proliferation of Oligo2+ progenitor cells following a CNS insult.
