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Maternal immune activation alters brain microRNA expression in mouse offspringopen access

Authors
Sunwoo, Jun-SangJeon, DaejongLee, Soon-TaeMoon, JangsupYu, Jung-SukPark, Dong-KyuBae, Ji-YeonLee, Doo YoungKim, SangwooJung, Keun-HwaPark, Kyung-IlJung, Ki-YoungKim, ManhoLee, Sang KunChu, Kon
Issue Date
Oct-2018
Publisher
John Wiley and Sons Ltd
Keywords
Maternal immune activation; microRNA; autism spectrum disorder
Citation
Annals of Clinical and Translational Neurology, v.5, no.10, pp 1264 - 1276
Pages
13
Journal Title
Annals of Clinical and Translational Neurology
Volume
5
Number
10
Start Page
1264
End Page
1276
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5610
DOI
10.1002/acn3.652
ISSN
2328-9503
Abstract
Objective: Maternal immune activation (MIA) is associated with an increased risk of autism spectrum disorder (ASD) in offspring. Herein, we investigate the altered expression of microRNAs (miRNA), and that of their target genes, in the brains of MIA mouse offspring. Methods: To generate MIA model mice, pregnant mice were injected with polyriboinosinic: polyribocytidylic acid on embryonic day 12.5. We performed miRNA microarray and mRNA sequencing in order to determine the differential expression of miRNA and mRNA between MIA mice and controls, at 3 weeks of age. We further identified predicted target genes of dysregulated miRNAs, and miRNA-target interactions, based on the inverse correlation of their expression levels. Results: Mice prenatally subjected to MIA exhibited behavioral abnormalities typical of ASD, such as a lack of preference for social novelty and reduced prepulse inhibition. We found 29 differentially expressed miRNAs (8 upregulated and 21 downregulated) and 758 differentially expressed mRNAs (542 upregulated and 216 downregulated) in MIA offspring compared to controls. Based on expression levels of the predicted target genes, 18 downregulated miRNAs (340 target genes) and three upregulated miRNAs (60 target genes) were found to be significantly enriched among the differentially expressed genes. miRNA and target gene interactions were most significant between mmu-miR-466i-3p and Hfm1 (ATP-dependent DNA helicase homolog), and between mmu-miR-877-3p and Aqp6 (aquaporin 6). Interpretation: Our results provide novel information regarding miRNA expression changes and their putative targets in the early postnatal period of brain development. Further studies will be needed to evaluate potential pathogenic roles of the dysregulated miRNAs.
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