Bmi-1 Absence Causes Premature Brain Degeneration
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 oxidativ...
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282795/ |
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pubmed-32827952012-02-23 Bmi-1 Absence Causes Premature Brain Degeneration Cao, Guangliang Gu, Minxia Zhu, Min Gao, Junying Yin, Ying Marshall, Charles Xiao, Ming Ding, Jiong Miao, Dengshun Research Article 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. Public Library of Science 2012-02-20 /pmc/articles/PMC3282795/ /pubmed/22363787 http://dx.doi.org/10.1371/journal.pone.0032015 Text en Cao et al. http://creativecommons.org/licenses/by/4.0/ 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 properly credited. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Cao, Guangliang Gu, Minxia Zhu, Min Gao, Junying Yin, Ying Marshall, Charles Xiao, Ming Ding, Jiong Miao, Dengshun |
spellingShingle |
Cao, Guangliang Gu, Minxia Zhu, Min Gao, Junying Yin, Ying Marshall, Charles Xiao, Ming Ding, Jiong Miao, Dengshun Bmi-1 Absence Causes Premature Brain Degeneration |
author_facet |
Cao, Guangliang Gu, Minxia Zhu, Min Gao, Junying Yin, Ying Marshall, Charles Xiao, Ming Ding, Jiong Miao, Dengshun |
author_sort |
Cao, Guangliang |
title |
Bmi-1 Absence Causes Premature Brain Degeneration |
title_short |
Bmi-1 Absence Causes Premature Brain Degeneration |
title_full |
Bmi-1 Absence Causes Premature Brain Degeneration |
title_fullStr |
Bmi-1 Absence Causes Premature Brain Degeneration |
title_full_unstemmed |
Bmi-1 Absence Causes Premature Brain Degeneration |
title_sort |
bmi-1 absence causes premature brain degeneration |
description |
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. |
publisher |
Public Library of Science |
publishDate |
2012 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282795/ |
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1611507141419466752 |