Abstract
Bmi-1, a polycomb transcriptional repressor, is implicated in cell cycle regulation and cell senescence. Its absence results in generalized astrogliosis and epilepsy during the postnatal development, but the underlying mechanisms are poorly understood. Here, we demonstrate the occurrence of oxidative stress in the brain of four-week-old Bmi-1 null mice. The mice showed various hallmarks of neurodegeneration including synaptic loss, axonal demyelination, reactive gliosis and brain mitochondrial damage. Moreover, astroglial glutamate transporters and glutamine synthetase decreased in the Bmi-1 null hippocampus, which might contribute to the sporadic epileptic-like seizures in these mice. These results indicate that Bmi-1 is required for maintaining endogenous antioxidant defenses in the brain, and its absence subsequently causes premature brain degeneration.
Document Type
Article
Publication Date
2-20-2012
Digital Object Identifier (DOI)
https://doi.org/10.1371/journal.pone.0032015
Funding Information
This work was supported by grants from the National Nature and Scientific Foundation of China Key Project (No. 30971020 to M. Xiao, No. 30830103 to D. Miao) and the Natural Science Foundation of Jiangsu Educational Department (09KJA310003 to M. Xiao).
Repository Citation
Cao, Guangliang; Gu, Minxia; Zhu, Min; Gao, Junying; Yin, Ying; Marshall, Charles; Xiao, Ming; Ding, Jiong; and Miao, Dengshun, "Bmi-1 Absence Causes Premature Brain Degeneration" (2012). Physical Therapy Faculty Publications. 9.
https://uknowledge.uky.edu/rehabsci_facpub/9
Supporting documents
Notes/Citation Information
Published in PLoS ONE, v. 7, no. 2, e32015, p. 1-9.
© 2012 Cao et al.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
There was an error in the Author Contributions section. The second contributions category should read: "Performed the experiments: GC MG MZ; GC and MG contributed equally to this work."