Alterations in Retrotransposition, Synaptic Connectivity, and Myelination Implicated by Transcriptomic Changes Following Maternal Immune Activation in Nonhuman Primates.

Tytuł:: Alterations in Retrotransposition, Synaptic Connectivity, and Myelination Implicated by Transcriptomic Changes Following Maternal Immune Activation in Nonhuman Primates.
Autorzy:: Page NF; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California; Department of Cell Biology and Neuroscience, Rutgers University-New Brunswick, Piscataway, New Jersey.
Gandal MJ; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California.
Estes ML; Center for Neuroscience, School of Medicine, University of California, Davis, Davis, California.
Cameron S; Center for Neuroscience, School of Medicine, University of California, Davis, Davis, California.
Buth J; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California; Program in Neurobehavioral Genetics, Center for Autism Research and Treatment, Los Angeles, California.
Parhami S; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California; Program in Neurobehavioral Genetics, Center for Autism Research and Treatment, Los Angeles, California.
Ramaswami G; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California; Program in Neurobehavioral Genetics, Center for Autism Research and Treatment, Los Angeles, California.
Murray K; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Amaral DG; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Van de Water JA; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Schumann CM; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Carter CS; Center for Neuroscience, School of Medicine, University of California, Davis, Davis, California; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Bauman MD; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
McAllister AK; Center for Neuroscience, School of Medicine, University of California, Davis, Davis, California; Department of Psychiatry and Behavioral Sciences, School of Medicine, University of California, Davis, Davis, California.
Geschwind DH; Department of Psychiatry, Center for Autism Research and Treatment, Los Angeles, California; Program in Neurobehavioral Genetics, Center for Autism Research and Treatment, Los Angeles, California; Department of Neurology, Center for Autism Research and Treatment, Los Angeles, California; Department of Human Genetics, Semel Institute, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California. Electronic address: .
Źródło:: Biological psychiatry [Biol Psychiatry] 2021 May 01; Vol. 89 (9), pp. 896-910. Date of Electronic Publication: 2020 Nov 02.
Typ publikacji:: Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: New York, NY : Elsevier
Original Publication: New York, Plenum Pub. Corp.
MeSH Terms:: Behavior, Animal*
Prenatal Exposure Delayed Effects*
Animals ; Argonaute Proteins ; Disease Models, Animal ; Female ; Humans ; Poly I-C ; Pregnancy ; Primates ; Transcriptome
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Grant Information:: P50 HD103526 United States HD NICHD NIH HHS; P50 HD103557 United States HD NICHD NIH HHS; P50 MH106438 United States MH NIMH NIH HHS
Contributed Indexing:: Keywords: MIA; Myelination; Nonhuman primates; RNA-seq; Retrotransposition; Synaptic connectivity
Substance Nomenclature:: 0 (Argonaute Proteins)
0 (PIWIL2 protein, human)
O84C90HH2L (Poly I-C)
Entry Date(s):: Date Created: 20210102 Date Completed: 20210423 Latest Revision: 20240312
Update Code:: 20240312
PubMed Central ID:: PMC8052273
DOI:: 10.1016/j.biopsych.2020.10.016
PMID:: 33386132
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Background: Maternal immune activation (MIA) is a proposed risk factor for multiple neuropsychiatric disorders, including schizophrenia. However, the molecular mechanisms through which MIA imparts risk remain poorly understood. A recently developed nonhuman primate model of exposure to the viral mimic poly:ICLC during pregnancy shows abnormal social and repetitive behaviors and elevated striatal dopamine, a molecular hallmark of human psychosis, providing an unprecedented opportunity for studying underlying molecular correlates.
Methods: We performed RNA sequencing across psychiatrically relevant brain regions (prefrontal cortex, anterior cingulate, hippocampus) and primary visual cortex for comparison from 3.5- to 4-year-old male MIA-exposed and control offspring-an age comparable to mid adolescence in humans.
Results: We identify 266 unique genes differentially expressed in at least one brain region, with the greatest number observed in hippocampus. Co-expression networks identified region-specific alterations in synaptic signaling and oligodendrocytes. Although we observed temporal and regional differences, transcriptomic changes were shared across first- and second-trimester exposures, including for the top differentially expressed genes-PIWIL2 and MGARP. In addition to PIWIL2, several other regulators of retrotransposition and endogenous transposable elements were dysregulated following MIA, potentially connecting MIA to retrotransposition.
Conclusions: Together, these results begin to elucidate the brain-level molecular processes through which MIA may impart risk for psychiatric disease.
(Copyright © 2020 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Comment in: Biol Psychiatry. 2021 May 1;89(9):842-844. (PMID: 33858590)

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