Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone

<p dir="ltr">Schizophrenia is a neurodevelopmental disorder likely caused by environmental and genetic risk factors but functional interactions between the risk factors are unclear. We tested the hypothesis that dysbindin-1 (Dtnbp1) gene mutation combined with postnatal exposure to v...

وصف كامل

محفوظ في:
التفاصيل البيبلوغرافية
المؤلف الرئيسي: Abeer R. Al-Shammari (11405339) (author)
مؤلفون آخرون: Sanjeev K. Bhardwaj (288221) (author), Ksenia Musaelyan (8670873) (author), Lalit K. Srivastava (13881896) (author), Francis G. Szele (9463190) (author)
منشور في: 2018
الموضوعات:
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author Abeer R. Al-Shammari (11405339)
author2 Sanjeev K. Bhardwaj (288221)
Ksenia Musaelyan (8670873)
Lalit K. Srivastava (13881896)
Francis G. Szele (9463190)
author2_role author
author
author
author
author_facet Abeer R. Al-Shammari (11405339)
Sanjeev K. Bhardwaj (288221)
Ksenia Musaelyan (8670873)
Lalit K. Srivastava (13881896)
Francis G. Szele (9463190)
author_role author
dc.creator.none.fl_str_mv Abeer R. Al-Shammari (11405339)
Sanjeev K. Bhardwaj (288221)
Ksenia Musaelyan (8670873)
Lalit K. Srivastava (13881896)
Francis G. Szele (9463190)
dc.date.none.fl_str_mv 2018-07-23T03:00:00Z
dc.identifier.none.fl_str_mv 10.1038/s41537-018-0057-5
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Schizophrenia-related_dysbindin-1_gene_is_required_for_innate_immune_response_and_homeostasis_in_the_developing_subventricular_zone/27050362
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biomedical and clinical sciences
Clinical sciences
Neurosciences
Behavioral changes
Inflammation
Subventricular zone (SVZ)
Prepulse inhibition
Locomotion
Novel object recognition
dc.title.none.fl_str_mv Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p dir="ltr">Schizophrenia is a neurodevelopmental disorder likely caused by environmental and genetic risk factors but functional interactions between the risk factors are unclear. We tested the hypothesis that dysbindin-1 (Dtnbp1) gene mutation combined with postnatal exposure to viral mimetic polyI:C results in schizophrenia-related behavioural changes in adulthood, and mediates polyI:C-induced inflammation in the subventricular zone (SVZ). Adult Sandy (Sdy, Dtnbp1 mutant) mice given early postnatal polyI:C injections displayed reduced prepulse inhibition of startle, reduced locomotion and deficits in novel object recognition. PolyI:C induced a canonical immune response in the SVZ; it increased mRNA expression of its toll-like receptor 3 (Tlr3) and downstream transcription factors RelA and Sp1. PolyI:C also increased SVZ Dtnbp1 mRNA expression, suggesting dysbindin-1 regulates immune responses. Dysbindin-1 loss in Sdy mice blocked the polyI:C-induced increases in mRNA expression of Tlr3, RelA and Sp1 in the SVZ. Dtnbp1 overexpression in SVZ-derived Sdy neurospheres rescued Tlr3, RelA and Sp1 mRNA expression supporting a functional interaction between dysbindin-1 and polyI:C-induced inflammation. Immunohistochemistry showed higher Iba1+ immune cell density in the SVZ of Sdy mice than in WT postnatally. PolyI:C did not alter SVZ Iba1+ cell density but increased CD45+/Iba1− cell numbers in the SVZ of Sdy mice. Finally, polyI:C injections in Sdy, but not WT mice reduced postnatal and adult SVZ proliferation. Together, we show novel functional interactions between the schizophrenia-relevant dysbindin-1 gene and the immune response to polyI:C. This work sheds light on the molecular basis for amplified abnormalities due to combined genetic predisposition and exposure to environmental schizophrenia risk factors.</p><h2>Other Information</h2><p dir="ltr">Published in: npj Schizophrenia<br>License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1038/s41537-018-0057-5" target="_blank">https://dx.doi.org/10.1038/s41537-018-0057-5</a></p>
eu_rights_str_mv openAccess
id Manara2_53dd4c271c75666daf3fdc4da81c26f1
identifier_str_mv 10.1038/s41537-018-0057-5
network_acronym_str Manara2
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oai_identifier_str oai:figshare.com:article/27050362
publishDate 2018
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spelling Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zoneAbeer R. Al-Shammari (11405339)Sanjeev K. Bhardwaj (288221)Ksenia Musaelyan (8670873)Lalit K. Srivastava (13881896)Francis G. Szele (9463190)Biomedical and clinical sciencesClinical sciencesNeurosciencesBehavioral changesInflammationSubventricular zone (SVZ)Prepulse inhibitionLocomotionNovel object recognition<p dir="ltr">Schizophrenia is a neurodevelopmental disorder likely caused by environmental and genetic risk factors but functional interactions between the risk factors are unclear. We tested the hypothesis that dysbindin-1 (Dtnbp1) gene mutation combined with postnatal exposure to viral mimetic polyI:C results in schizophrenia-related behavioural changes in adulthood, and mediates polyI:C-induced inflammation in the subventricular zone (SVZ). Adult Sandy (Sdy, Dtnbp1 mutant) mice given early postnatal polyI:C injections displayed reduced prepulse inhibition of startle, reduced locomotion and deficits in novel object recognition. PolyI:C induced a canonical immune response in the SVZ; it increased mRNA expression of its toll-like receptor 3 (Tlr3) and downstream transcription factors RelA and Sp1. PolyI:C also increased SVZ Dtnbp1 mRNA expression, suggesting dysbindin-1 regulates immune responses. Dysbindin-1 loss in Sdy mice blocked the polyI:C-induced increases in mRNA expression of Tlr3, RelA and Sp1 in the SVZ. Dtnbp1 overexpression in SVZ-derived Sdy neurospheres rescued Tlr3, RelA and Sp1 mRNA expression supporting a functional interaction between dysbindin-1 and polyI:C-induced inflammation. Immunohistochemistry showed higher Iba1+ immune cell density in the SVZ of Sdy mice than in WT postnatally. PolyI:C did not alter SVZ Iba1+ cell density but increased CD45+/Iba1− cell numbers in the SVZ of Sdy mice. Finally, polyI:C injections in Sdy, but not WT mice reduced postnatal and adult SVZ proliferation. Together, we show novel functional interactions between the schizophrenia-relevant dysbindin-1 gene and the immune response to polyI:C. This work sheds light on the molecular basis for amplified abnormalities due to combined genetic predisposition and exposure to environmental schizophrenia risk factors.</p><h2>Other Information</h2><p dir="ltr">Published in: npj Schizophrenia<br>License: <a href="https://creativecommons.org/licenses/by/4.0" target="_blank">https://creativecommons.org/licenses/by/4.0</a><br>See article on publisher's website: <a href="https://dx.doi.org/10.1038/s41537-018-0057-5" target="_blank">https://dx.doi.org/10.1038/s41537-018-0057-5</a></p>2018-07-23T03:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1038/s41537-018-0057-5https://figshare.com/articles/journal_contribution/Schizophrenia-related_dysbindin-1_gene_is_required_for_innate_immune_response_and_homeostasis_in_the_developing_subventricular_zone/27050362CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/270503622018-07-23T03:00:00Z
spellingShingle Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
Abeer R. Al-Shammari (11405339)
Biomedical and clinical sciences
Clinical sciences
Neurosciences
Behavioral changes
Inflammation
Subventricular zone (SVZ)
Prepulse inhibition
Locomotion
Novel object recognition
status_str publishedVersion
title Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
title_full Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
title_fullStr Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
title_full_unstemmed Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
title_short Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
title_sort Schizophrenia-related dysbindin-1 gene is required for innate immune response and homeostasis in the developing subventricular zone
topic Biomedical and clinical sciences
Clinical sciences
Neurosciences
Behavioral changes
Inflammation
Subventricular zone (SVZ)
Prepulse inhibition
Locomotion
Novel object recognition