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Article: Frontal-subcortical protein expression following prenatal exposure to maternal inflammation
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TitleFrontal-subcortical protein expression following prenatal exposure to maternal inflammation
 
AuthorsDeng, MY2
Lam, S2
Meyer, U1
Feldon, J1
Li, Q2
Wei, R2
Luk, L2
Chua, SE2 2
Sham, P2 2
Wang, Y2
McAlonan, GM2 2
 
KeywordsGuanine nucleotide binding protein
Lactate dehydrogenase
Mitogen activated protein kinase
Proteome
Protein expression
 
Issue Date2011
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2011, v. 6 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0016638
 
AbstractBackground: Maternal immune activation (MIA) during prenatal life is a risk factor for neurodevelopmental disorders including schizophrenia and autism. Such conditions are associated with alterations in fronto-subcortical circuits, but their molecular basis is far from clear. Methodology/Principal Findings: Using two-dimensional differential in-gel electrophoresis (2D-DIGE) and mass spectrometry, with targeted western blot analyses for confirmation, we investigated the impact of MIA on the prefrontal and striatal proteome from an established MIA mouse model generated in C57B6 mice, by administering the viral analogue PolyI:C or saline vehicle (control) intravenously on gestation day (GD) 9. In striatum, 11 proteins were up-regulated and 4 proteins were down-regulated in the PolyI:C mice, while 10 proteins were up-regulated and 7 proteins down-regulated in prefrontal cortex (PFC). These were proteins involved in the mitogen-activated protein kinase (MAPK) signaling pathway, oxidation and auto-immune targets, including dual specificity mitogen-activated protein kinase kinase 1 (MEK), eukaryotic initiation factor (eIF) 4A-II, creatine kinase (CK)-B, L-lactate dehydrogenase (LDH)-B, WD repeat-containing protein and NADH dehydrogenase in the striatum; and guanine nucleotide-binding protein (G-protein), 14-3-3 protein, alpha-enolase, olfactory maker protein and heat shock proteins (HSP) 60, and 90-beta in the PFC. Conclusions/Significance: This data fits with emerging evidence for disruption of critical converging intracellular pathways involving MAPK pathways in neurodevelopmental conditions and it shows considerable overlap with protein pathways identified by genetic modeling and clinical post-mortem studies. This has implications for understanding causality and may offer potential biomarkers and novel treatment targets for neurodevelopmental conditions. © 2011 Deng et al.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0016638
 
PubMed Central IDPMC3037372
 
ISI Accession Number IDWOS:000287363000011
Funding AgencyGrant Number
Swiss Federal Institute of Technology (ETH) Zurich1107/03
Swiss National Science Foundation3100AO-100309
3100A0-116719
NARSAD Distinguished Investigator Award
University of Hong Kong
Hong Kong Research Grants Council
Funding Information:

JF and UM received financial support from the Swiss Federal Institute of Technology (ETH) Zurich (grant-1107/03) and the Swiss National Science Foundation (grant 3100AO-100309 and grant 3100A0-116719). JF holds a 2009 NARSAD Distinguished Investigator Award. GMA was funded by a University of Hong Kong Award and holds a General Research Fund from the Hong Kong Research Grants Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorDeng, MY
 
dc.contributor.authorLam, S
 
dc.contributor.authorMeyer, U
 
dc.contributor.authorFeldon, J
 
dc.contributor.authorLi, Q
 
dc.contributor.authorWei, R
 
dc.contributor.authorLuk, L
 
dc.contributor.authorChua, SE
 
dc.contributor.authorSham, P
 
dc.contributor.authorWang, Y
 
dc.contributor.authorMcAlonan, GM
 
dc.date.accessioned2011-07-27T01:34:46Z
 
dc.date.available2011-07-27T01:34:46Z
 
dc.date.issued2011
 
dc.description.abstractBackground: Maternal immune activation (MIA) during prenatal life is a risk factor for neurodevelopmental disorders including schizophrenia and autism. Such conditions are associated with alterations in fronto-subcortical circuits, but their molecular basis is far from clear. Methodology/Principal Findings: Using two-dimensional differential in-gel electrophoresis (2D-DIGE) and mass spectrometry, with targeted western blot analyses for confirmation, we investigated the impact of MIA on the prefrontal and striatal proteome from an established MIA mouse model generated in C57B6 mice, by administering the viral analogue PolyI:C or saline vehicle (control) intravenously on gestation day (GD) 9. In striatum, 11 proteins were up-regulated and 4 proteins were down-regulated in the PolyI:C mice, while 10 proteins were up-regulated and 7 proteins down-regulated in prefrontal cortex (PFC). These were proteins involved in the mitogen-activated protein kinase (MAPK) signaling pathway, oxidation and auto-immune targets, including dual specificity mitogen-activated protein kinase kinase 1 (MEK), eukaryotic initiation factor (eIF) 4A-II, creatine kinase (CK)-B, L-lactate dehydrogenase (LDH)-B, WD repeat-containing protein and NADH dehydrogenase in the striatum; and guanine nucleotide-binding protein (G-protein), 14-3-3 protein, alpha-enolase, olfactory maker protein and heat shock proteins (HSP) 60, and 90-beta in the PFC. Conclusions/Significance: This data fits with emerging evidence for disruption of critical converging intracellular pathways involving MAPK pathways in neurodevelopmental conditions and it shows considerable overlap with protein pathways identified by genetic modeling and clinical post-mortem studies. This has implications for understanding causality and may offer potential biomarkers and novel treatment targets for neurodevelopmental conditions. © 2011 Deng et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2011, v. 6 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0016638
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0016638
 
dc.identifier.epagee16638
 
dc.identifier.hkuros187197
 
dc.identifier.isiWOS:000287363000011
Funding AgencyGrant Number
Swiss Federal Institute of Technology (ETH) Zurich1107/03
Swiss National Science Foundation3100AO-100309
3100A0-116719
NARSAD Distinguished Investigator Award
University of Hong Kong
Hong Kong Research Grants Council
Funding Information:

JF and UM received financial support from the Swiss Federal Institute of Technology (ETH) Zurich (grant-1107/03) and the Swiss National Science Foundation (grant 3100AO-100309 and grant 3100A0-116719). JF holds a 2009 NARSAD Distinguished Investigator Award. GMA was funded by a University of Hong Kong Award and holds a General Research Fund from the Hong Kong Research Grants Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue2
 
dc.identifier.pmcidPMC3037372
 
dc.identifier.pmid21347362
 
dc.identifier.scopuseid_2-s2.0-79951837281
 
dc.identifier.spagee16638
 
dc.identifier.urihttp://hdl.handle.net/10722/135404
 
dc.identifier.volume6
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subjectGuanine nucleotide binding protein
 
dc.subjectLactate dehydrogenase
 
dc.subjectMitogen activated protein kinase
 
dc.subjectProteome
 
dc.subjectProtein expression
 
dc.titleFrontal-subcortical protein expression following prenatal exposure to maternal inflammation
 
dc.typeArticle
 
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<contributor.author>Wei, R</contributor.author>
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<contributor.author>Chua, SE</contributor.author>
<contributor.author>Sham, P</contributor.author>
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<contributor.author>McAlonan, GM</contributor.author>
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Author Affiliations
  1. Eidgenossische Technische Hochschule Zurich
  2. The University of Hong Kong