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
Open accessAbstract
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.
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A reduced number of hippocampal and prefrontal parvalbumin-immunoreactive interneurons is observed in Schnurri-2 knockout mice, a genetic model for enhanced neuroinflammation via increased NF-kB-dependent gene expression.
“A reduced number of hippocampal and prefrontal parvalbumin-immunoreactive interneurons is also observed in Schnurri-2 KO mice, a genetic model for enhanced neuroinflammation via increased NF-kB-dependent gene expression (Takao et al., 2013).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Takao et al., 2013
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- Authors
- Takao, K., Kobayashi, K., Hagihara, H., Ohira, K., Shoji, H., Hattori, S., Koshimizu, H., Umemori, J., Toyama, K., Nakamura, H. K., Kuroiwa, M., Maeda, J., Atsuzawa, K., Esaki, K., Yamaguchi, S., Furuya, S., Takagi, T., Walton, N. M., Hayashi, N., Suzuki, H., Higuchi, M., Usuda, N., Suhara, T., Nishi, A., Matsumoto, M., Ishii, S., & Miyakawa, T.
- Affiliations
- Fujita Health University (JP)
- Japan Science and Technology Agency (JP)
- Kurume University (JP)
- National Institute of Radiological Sciences (JP)
- Kyushu University (JP)
- RIKEN (JP)
- Tokyo Institute of Technology (JP)
- Corresponding author
- Miyakawa, Tsuyoshi
- ORCID
- Takao, Keizo
- Kobayashi, Katsunori
- Hagihara, Hideo
- Ohira, Koji
- Shoji, Hirotaka
- Hattori, Satoko
- Koshimizu, Hisatsugu
- Umemori, Juzoh
- Toyama, Keiko
- Nakamura, Hironori K
- Maeda, Jun
- Atsuzawa, Kimie
- Esaki, Kayoko
- Furuya, Shigeki
- Takagi, Tsuyoshi
- Hayashi, Nobuhiro
- Suzuki, Hidenori
- Higuchi, Makoto
- Suhara, Tetsuya
- Nishi, Akinori
- Matsumoto, Mitsuyuki
- Ishii, Shunsuke
- Miyakawa, Tsuyoshi
- Venue
- Neuropsychopharmacology
- Published
- 2013-02-06
- Volume
- 38
- Issue
- 8
- Pages
- 1409-1425
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3682135
- OpenAlex
- W2025293038
- Cited by
- 173
- References
- 66
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 10 · 2023: 9 · 2022: 17 · 2021: 10 · 2020: 14 · 2019: 14 · 2018: 13 · 2017: 14 · 2016: 16 · 2015: 14 · 2014: 14 · 2013: 11
- FWCI
- 5.93
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (unspecified)
- Locations
- Neuropsychopharmacology (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- QST-Repository (National Institutes for Quantum and Radiological Science and Technology) (submittedVersion)
- Tokyo Tech Research Repository (Tokyo Institute of Technology) (submittedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology (18023022, 20023017, 17025023, 24111546, CREST)
- National Institute of Biomedical Innovation (17025023, 20023017, 24111546, 18023022)
- Japan Society for the Promotion of Science (221S0003, 22651075, 20023017, 23390235, 24791244, 23370079, 17025023, CREST, 18023022, 23792018, 22380078, 24657008, 24111546)
- Japan Science and Technology Agency (18023022, CREST, 20023017, 17025023, 24111546)
- Core Research for Evolutional Science and Technology
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- schizophrenia, neuroinflammation, parvalbumin, GAD67, working memory, nest building behavior, anti-inflammatory agents, glial fibrillary acidic protein, NADPH oxidase p22phox, endophenotypes
- MeSH terms
- Animals, Brain, Chronic Disease, DNA-Binding Proteins, Inflammation, Mice, Inbred BALB C, Mice, Inbred C57BL, Neurons, Phenotype, Schizophrenia, Mice, Knockout, Mice
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