| Item type |
文献 / Documents(1) |
| 公開日 |
2024-10-11 |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| item_1722929371688 |
|
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|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.1371/journal.pone.0013083 |
|
|
言語 |
ja |
|
|
関連名称 |
10.1371/journal.pone.0013083 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Delayed Onset of Experimental Autoimmune Encephalomyelitis in Olig1 Deficient Mice |
|
言語 |
en |
| タイトル別表記 |
|
|
その他のタイトル |
Role of Oligl in EAE |
|
言語 |
en |
| 著者 |
Guo, Xiaoli
Harada, Chikako
Namekata, Kazuhiko
三田村, 佳典
Yoshida, Hiroshi
Matsumoto, Yoh
Harada, Takayuki
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Background: Olig1 is a basic helix-loop-helix (bHLH) transcription factor that is essential for oligodendrogenesis and efficient remyelination. However, its role in neurodegenerative disorders has not been well-elucidated.
Methodology/Principal Findings: Here we investigated the effects of Olig1 deficiency on experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). We show that the mean disease onset of myelin oligodendrocyte glycoprotein (MOG)-induced EAE in Olig1−/− mice is significantly slower than wide-type (WT) mice (19.8±2.2 in Olig1−/− mice and 9.5±0.3 days in WT mice). In addition, 10% of Olig1−/− mice did not develop EAE by the end of the observation periods (60 days). The severity of EAE, the extent of demyelination, and the activation of microglial cells and astrocytes in spinal cords, were significantly milder in Olig1−/− mice compared with WT mice in the early stage. Moreover, the visual function, as assessed by the second-kernel of multifocal electroretinograms, was better preserved, and the number of degenerating axons in the optic nerve was significantly reduced in Olig1−/− mice. Interestingly, Olig1 deficiency had no effect on T cell response capability, however, it reduced the expression of myelin proteins such as MOG, myelin basic protein (MBP) and myelin-associated glycoprotein (MAG). The expression of Olig2 remained unchanged in the optic nerve and brain, and it was reduced in the spinal cord of Olig1−/− mice.
Conclusions/Significance: Our results suggest that the Olig1 signaling pathways may be involved in the incidence rate and the severity of neurological symptoms in MS. |
|
言語 |
en |
| bibliographic_information |
en : PLOS ONE
巻 5,
号 9,
p. e13083,
発行日 2010-09-29
|
| 収録物ID |
|
|
収録物識別子タイプ |
EISSN |
|
収録物識別子 |
19326203 |
| 出版者 |
|
|
出版者 |
PLOS |
|
言語 |
en |
| item_10001_rights_15 |
|
|
言語 |
en |
|
権利情報 |
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. |
| item_1723180141928 |
|
|
識別子 |
222705 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
pone_5_9_e13083.pdf (9.9 MB)
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