Abnormal expression of myelination genes and alterations in white matter fractional anisotropy following prenatal viral influenza infection at E16 in mice

S. Hossein Fatemi, Timothy D. Folsom, Teri J. Reutiman, Desiree Abu-Odeh, Susumu Mori, Hao Huang, Kenichi Oishi

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

Prenatal viral infection has been associated with the development of schizophrenia and autism. Our laboratory has previously shown that viral infection causes deleterious effects on brain structure and function in mouse offspring following late first trimester (E9) and late second trimester (E18) administration of influenza virus. We hypothesized that middle second trimester infection (E16) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring. C57BL6 mice were infected on E16 with a sublethal dose of human influenza virus or sham-infected using vehicle solution. Male offspring of the infected mice were collected at P0, P14, P35, and P56, their brains removed and cerebella dissected and flash frozen. Microarray, DTI and MRI scanning, as well as qRT-PCR and SDS-PAGE and western blotting analyses were performed to detect differences in gene expression and brain atrophy. Expression of several genes associated with myelination, including Mbp, Mag, and Plp1 were found to be altered, as were protein levels of Mbp, Mag, and DM20. Brain imaging revealed significant atrophy in cerebellum at P14, reduced fractional anisotropy in white matter of the right internal capsule at P0, and increased fractional anisotropy in white matter in corpus callosum at P14 and right middle cerebellar peduncle at P56. We propose that maternal infection in mouse impacts myelination genes.

Original languageEnglish (US)
Pages (from-to)46-53
Number of pages8
JournalSchizophrenia Research
Volume112
Issue number1-3
DOIs
StatePublished - Jul 2009

Fingerprint

Anisotropy
Virus Diseases
Human Influenza
Gene Expression
Brain
Second Pregnancy Trimester
Orthomyxoviridae
Cerebellum
Atrophy
Internal Capsule
Corpus Callosum
First Pregnancy Trimester
Autistic Disorder
Infection
Neuroimaging
Polyacrylamide Gel Electrophoresis
Schizophrenia
Western Blotting
Mothers
White Matter

Keywords

  • Autism
  • Brain
  • Mouse
  • Myelination
  • Schizophrenia
  • Viral model

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry

Cite this

Abnormal expression of myelination genes and alterations in white matter fractional anisotropy following prenatal viral influenza infection at E16 in mice. / Fatemi, S. Hossein; Folsom, Timothy D.; Reutiman, Teri J.; Abu-Odeh, Desiree; Mori, Susumu; Huang, Hao; Oishi, Kenichi.

In: Schizophrenia Research, Vol. 112, No. 1-3, 07.2009, p. 46-53.

Research output: Contribution to journalArticle

Fatemi, S. Hossein ; Folsom, Timothy D. ; Reutiman, Teri J. ; Abu-Odeh, Desiree ; Mori, Susumu ; Huang, Hao ; Oishi, Kenichi. / Abnormal expression of myelination genes and alterations in white matter fractional anisotropy following prenatal viral influenza infection at E16 in mice. In: Schizophrenia Research. 2009 ; Vol. 112, No. 1-3. pp. 46-53.
@article{e955e647e78a4529843339603a92c810,
title = "Abnormal expression of myelination genes and alterations in white matter fractional anisotropy following prenatal viral influenza infection at E16 in mice",
abstract = "Prenatal viral infection has been associated with the development of schizophrenia and autism. Our laboratory has previously shown that viral infection causes deleterious effects on brain structure and function in mouse offspring following late first trimester (E9) and late second trimester (E18) administration of influenza virus. We hypothesized that middle second trimester infection (E16) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring. C57BL6 mice were infected on E16 with a sublethal dose of human influenza virus or sham-infected using vehicle solution. Male offspring of the infected mice were collected at P0, P14, P35, and P56, their brains removed and cerebella dissected and flash frozen. Microarray, DTI and MRI scanning, as well as qRT-PCR and SDS-PAGE and western blotting analyses were performed to detect differences in gene expression and brain atrophy. Expression of several genes associated with myelination, including Mbp, Mag, and Plp1 were found to be altered, as were protein levels of Mbp, Mag, and DM20. Brain imaging revealed significant atrophy in cerebellum at P14, reduced fractional anisotropy in white matter of the right internal capsule at P0, and increased fractional anisotropy in white matter in corpus callosum at P14 and right middle cerebellar peduncle at P56. We propose that maternal infection in mouse impacts myelination genes.",
keywords = "Autism, Brain, Mouse, Myelination, Schizophrenia, Viral model",
author = "Fatemi, {S. Hossein} and Folsom, {Timothy D.} and Reutiman, {Teri J.} and Desiree Abu-Odeh and Susumu Mori and Hao Huang and Kenichi Oishi",
year = "2009",
month = "7",
doi = "10.1016/j.schres.2009.04.014",
language = "English (US)",
volume = "112",
pages = "46--53",
journal = "Schizophrenia Research",
issn = "0920-9964",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Abnormal expression of myelination genes and alterations in white matter fractional anisotropy following prenatal viral influenza infection at E16 in mice

AU - Fatemi, S. Hossein

AU - Folsom, Timothy D.

AU - Reutiman, Teri J.

AU - Abu-Odeh, Desiree

AU - Mori, Susumu

AU - Huang, Hao

AU - Oishi, Kenichi

PY - 2009/7

Y1 - 2009/7

N2 - Prenatal viral infection has been associated with the development of schizophrenia and autism. Our laboratory has previously shown that viral infection causes deleterious effects on brain structure and function in mouse offspring following late first trimester (E9) and late second trimester (E18) administration of influenza virus. We hypothesized that middle second trimester infection (E16) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring. C57BL6 mice were infected on E16 with a sublethal dose of human influenza virus or sham-infected using vehicle solution. Male offspring of the infected mice were collected at P0, P14, P35, and P56, their brains removed and cerebella dissected and flash frozen. Microarray, DTI and MRI scanning, as well as qRT-PCR and SDS-PAGE and western blotting analyses were performed to detect differences in gene expression and brain atrophy. Expression of several genes associated with myelination, including Mbp, Mag, and Plp1 were found to be altered, as were protein levels of Mbp, Mag, and DM20. Brain imaging revealed significant atrophy in cerebellum at P14, reduced fractional anisotropy in white matter of the right internal capsule at P0, and increased fractional anisotropy in white matter in corpus callosum at P14 and right middle cerebellar peduncle at P56. We propose that maternal infection in mouse impacts myelination genes.

AB - Prenatal viral infection has been associated with the development of schizophrenia and autism. Our laboratory has previously shown that viral infection causes deleterious effects on brain structure and function in mouse offspring following late first trimester (E9) and late second trimester (E18) administration of influenza virus. We hypothesized that middle second trimester infection (E16) in mice may lead to a different pattern of brain gene expression and structural defects in the developing offspring. C57BL6 mice were infected on E16 with a sublethal dose of human influenza virus or sham-infected using vehicle solution. Male offspring of the infected mice were collected at P0, P14, P35, and P56, their brains removed and cerebella dissected and flash frozen. Microarray, DTI and MRI scanning, as well as qRT-PCR and SDS-PAGE and western blotting analyses were performed to detect differences in gene expression and brain atrophy. Expression of several genes associated with myelination, including Mbp, Mag, and Plp1 were found to be altered, as were protein levels of Mbp, Mag, and DM20. Brain imaging revealed significant atrophy in cerebellum at P14, reduced fractional anisotropy in white matter of the right internal capsule at P0, and increased fractional anisotropy in white matter in corpus callosum at P14 and right middle cerebellar peduncle at P56. We propose that maternal infection in mouse impacts myelination genes.

KW - Autism

KW - Brain

KW - Mouse

KW - Myelination

KW - Schizophrenia

KW - Viral model

UR - http://www.scopus.com/inward/record.url?scp=67349188747&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67349188747&partnerID=8YFLogxK

U2 - 10.1016/j.schres.2009.04.014

DO - 10.1016/j.schres.2009.04.014

M3 - Article

VL - 112

SP - 46

EP - 53

JO - Schizophrenia Research

JF - Schizophrenia Research

SN - 0920-9964

IS - 1-3

ER -