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Prostaglandin E2 Reverses Aberrant Production of an Inflammatory Chemokine by Microglia from Sandhoff Disease Model Mice through the cAMP-PKA Pathway
https://tokushima-u.repo.nii.ac.jp/records/2000222
https://tokushima-u.repo.nii.ac.jp/records/200022234934492-464b-4f8e-a7db-489992374fb7
| 名前 / ファイル | ライセンス | アクション |
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pone_6_1_e16269.pdf (521 KB)
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| Item type | 文献 / Documents(1) | |||||||||||||||||||
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| 公開日 | 2024-10-16 | |||||||||||||||||||
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| 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 | |||||||||||||||||||
| 出版社版DOI | ||||||||||||||||||||
| 関連識別子 | https://doi.org/10.1371/journal.pone.0016269 | |||||||||||||||||||
| 関連名称 | 10.1371/journal.pone.0016269 | |||||||||||||||||||
| 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 | Prostaglandin E2 Reverses Aberrant Production of an Inflammatory Chemokine by Microglia from Sandhoff Disease Model Mice through the cAMP-PKA Pathway | |||||||||||||||||||
| タイトル別表記 | ||||||||||||||||||||
| その他のタイトル | Down-Regulation of MIP-1 by PGE2 in SD Microglia | |||||||||||||||||||
| 著者 |
Kawashita, Eri
× Kawashita, Eri
× 辻, 大輔× Toyoshima, Masahiro
× Kanno, Yosuke
× Matsuno, Hiroyuki
× 伊藤, 孝司
WEKO
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| 内容記述 | Background: Sandhoff disease (SD) is a neurodegenerative lysosomal β-hexosaminidase (Hex) deficiency involving excessive accumulation of undegraded substrates, including terminal GlcNAc-oligosaccharides and GM2 ganglioside. Microglia-mediated neuroinflammation contributes to the pathogenesis and progression of SD. Our previous study demonstrated that MIP-1α, a putative pathogenic factor for SD, is up-regulated in microglial cells derived from SD model mice (SD-Mg) through activation of Akt and JNK. Methodology/Principal Findings: In this study, we first demonstrated that prostaglandin E2 (PGE2), which is one of the lipid mediators derived from arachidonic acid and is known to suppress activation of microglia, reduced the aberrant MIP-1α production by SD-Mg to the same level as by WT-Mg. PGE2 also attenuated the activation of Akt and JNK. The inhibition of MIP-1α production and the activation of Akt and JNK occurred through the EP2 and 4/cAMP/PKA signaling pathway in the murine microglia derived from SD model mice. Conclusions/Significance: We propose that PGE2 plays a role as a negative regulator of MIP-1α production in the pathogenesis of SD, and that PGE2-EP2 and 4/cAMP/PKA signaling could be a target pathway for therapy for SD. |
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| 書誌情報 |
en : PLOS ONE 巻 6, 号 1, p. e16269, 発行日 2011-01-27 |
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| 収録物識別子タイプ | EISSN | |||||||||||||||||||
| 収録物識別子 | 19326203 | |||||||||||||||||||
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| 出版者 | PLOS | |||||||||||||||||||
| 権利情報 | ||||||||||||||||||||
| 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. | |||||||||||||||||||
| EID | ||||||||||||||||||||
| 識別子 | 222234 | |||||||||||||||||||
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| 言語 | eng | |||||||||||||||||||
