WEKO3
アイテム
Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.
https://repo.qst.go.jp/records/46878
https://repo.qst.go.jp/records/46878b6410569-645b-4620-b024-2789e02d4185
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2014-10-21 | |||||
| タイトル | ||||||
| タイトル | Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 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 | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Takao, Keizo
× Takao, Keizo× Kobayashi, Katsunori× Hagihara, Hideo× Ohira, Koji× Shoji, Hirotaka× Hattori, Satoko× Koshimizu, Hisatsugu× Umemori, Juzoh× Toyama, Keiko× K, Nakamura Hironori× Kuroiwa, Mahomi× Maeda, Jun× Atsuzawa, Kimie× Esaki, Kayoko× Yamaguchi, Shun× Furuya, Shigeki× Takagi, Tsuyoshi× M, Walton Noah× Hayashi, Nobuhiro× Suzuki, Hidenori× Higuchi, Makoto× Usuda, Nobuteru× Suhara, Tetsuya× Nishi, Akinori× Matsumoto, Mitsuyuki× Ishii, Shunsuke× Miyakawa, Tsuyoshi× 前田 純× 樋口 真人× 須原 哲也 |
|||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Schnurri-2 (Shn-2), an nuclear factor-κB site-binding protein, tightly binds to the enhancers of major histocompatibility complex class I genes and inflammatory cytokines, which have been shown to harbor common variant single-nucleotide polymorphisms associated with schizophrenia. Although genes related to immunity are implicated in schizophrenia, there has been no study showing that their mutation or knockout (KO) results in schizophrenia. Here, we show that Shn-2 KO mice have behavioral abnormalities that resemble those of schizophrenics. The mutant brain demonstrated multiple schizophrenia-related phenotypes, including transcriptome/proteome changes similar to those of postmortem schizophrenia patients, decreased parvalbumin and GAD67 levels, increased theta power on electroencephalograms, and a thinner cortex. Dentate gyrus granule cells failed to mature in mutants, a previously proposed endophenotype of schizophrenia. Shn-2 KO mice also exhibited mild chronic inflammation of the brain, as evidenced by increased inflammation markers (including GFAP and NADH/NADPH oxidase p22 phox), and genome-wide gene expression patterns similar to various inflammatory conditions. Chronic administration of anti-inflammatory drugs reduced hippocampal GFAP expression, and reversed deficits in working memory and nest-building behaviors in Shn-2 KO mice. These results suggest that genetically induced changes in immune system can be a predisposing factor in schizophrenia. | |||||
| 書誌情報 |
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 巻 38, 号 8, p. 1409-1425, 発行日 2013-02 |
|||||
| 出版者 | ||||||
| 出版者 | Nature Publishing Group | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0006-3223 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 23389689 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1038/npp.2013.38 | |||||
