Endogenous Circadian Clock Machinery in Cortical NG2-Glia Regulates Cellular Proliferation


Journal article


Terry Dean, Aissia Victoria Koffi, Evan Z. Goldstein, Javid Ghaemmaghami, V. Gallo
eNeuro, 2022

Semantic Scholar DOI PubMedCentral PubMed
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APA   Click to copy
Dean, T., Koffi, A. V., Goldstein, E. Z., Ghaemmaghami, J., & Gallo, V. (2022). Endogenous Circadian Clock Machinery in Cortical NG2-Glia Regulates Cellular Proliferation. ENeuro.


Chicago/Turabian   Click to copy
Dean, Terry, Aissia Victoria Koffi, Evan Z. Goldstein, Javid Ghaemmaghami, and V. Gallo. “Endogenous Circadian Clock Machinery in Cortical NG2-Glia Regulates Cellular Proliferation.” eNeuro (2022).


MLA   Click to copy
Dean, Terry, et al. “Endogenous Circadian Clock Machinery in Cortical NG2-Glia Regulates Cellular Proliferation.” ENeuro, 2022.


BibTeX   Click to copy

@article{terry2022a,
  title = {Endogenous Circadian Clock Machinery in Cortical NG2-Glia Regulates Cellular Proliferation},
  year = {2022},
  journal = {eNeuro},
  author = {Dean, Terry and Koffi, Aissia Victoria and Goldstein, Evan Z. and Ghaemmaghami, Javid and Gallo, V.}
}

Abstract

Abstract The molecular circadian clock can be found throughout the body and is essential for the synchronizing cellular physiology with the 24 h day. However, the role of the clock in regulating the regenerative potential of the brain has not been explored. We report here that murine NG2-glia, the largest population of proliferative cells in the mature central nervous system, rhythmically express circadian clock genes in a 24 h period, including the critical clock component Bmal1 RNA and BMAL1 protein. Interestingly, daily NG2-glia proliferation preferentially occurs during the time of day in which Bmal1 expression is high, while conditional knockout of Bmal1 decreases both cortical NG2-glia density and cellular proliferation. Furthermore, in a neurotrauma model, we show that pathology-induced NG2-glia proliferation is also dependent on Bmal1 expression. Because circadian rhythm disturbances are common in neurologic disorders across the life span, including in traumatic brain injury, these findings bear significant implications for cellular regeneration in brain injuries and disease.


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