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Article: Frontal-subcortical protein expression following prenatal exposure to maternal inflammation

TitleFrontal-subcortical protein expression following prenatal exposure to maternal inflammation
Authors
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
Citation
Plos One, 2011, v. 6 n. 2 How to Cite?
Abstract
Background: 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.
Persistent Identifierhttp://hdl.handle.net/10722/135404
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
PubMed Central ID
ISI Accession Number ID
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.

References

 

Author Affiliations
  1. Eidgenossische Technische Hochschule Zurich
  2. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorDeng, MYen_HK
dc.contributor.authorLam, Sen_HK
dc.contributor.authorMeyer, Uen_HK
dc.contributor.authorFeldon, Jen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorWei, Ren_HK
dc.contributor.authorLuk, Len_HK
dc.contributor.authorChua, SEen_HK
dc.contributor.authorSham, Pen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorMcAlonan, GMen_HK
dc.date.accessioned2011-07-27T01:34:46Z-
dc.date.available2011-07-27T01:34:46Z-
dc.date.issued2011en_HK
dc.identifier.citationPlos One, 2011, v. 6 n. 2en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/135404-
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.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
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 inflammationen_HK
dc.typeArticleen_HK
dc.identifier.emailSham, P: pcsham@hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hken_HK
dc.identifier.authoritySham, P=rp00459en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityMcAlonan, GM=rp00475en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0016638en_HK
dc.identifier.pmid21347362-
dc.identifier.pmcidPMC3037372-
dc.identifier.scopuseid_2-s2.0-79951837281en_HK
dc.identifier.hkuros187197en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79951837281&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume6en_HK
dc.identifier.issue2en_HK
dc.identifier.spagee16638en_US
dc.identifier.epagee16638en_US
dc.identifier.isiWOS:000287363000011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDeng, MY=35336436100en_HK
dc.identifier.scopusauthoridLam, S=39861665000en_HK
dc.identifier.scopusauthoridMeyer, U=35196427300en_HK
dc.identifier.scopusauthoridFeldon, J=7102146902en_HK
dc.identifier.scopusauthoridLi, Q=36062654700en_HK
dc.identifier.scopusauthoridWei, R=34769199800en_HK
dc.identifier.scopusauthoridLuk, L=37016576200en_HK
dc.identifier.scopusauthoridChua, SE=37016141500en_HK
dc.identifier.scopusauthoridSham, P=34573429300en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridMcAlonan, GM=6603123011en_HK

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