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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Main Authors: Cao, Guangliang, Gu, Minxia, Zhu, Min, Gao, Junying, Yin, Ying, Marshall, Charles, Xiao, Ming, Ding, Jiong, Miao, Dengshun
Format: Online
Language:English
Published: Public Library of Science 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282795/
id pubmed-3282795
recordtype oai_dc
spelling 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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