scholarly journals tRNA-derived fragments and microRNAs in the maternal-fetal interface of a mouse maternal-immune-activation autism model

2019 ◽  
Author(s):  
Zhangli Su ◽  
Elizabeth L. Frost ◽  
Catherine R. Lammert ◽  
Roza K. Przanowska ◽  
John R. Lukens ◽  
...  
Keyword(s):  
Environmental Stress ◽  
Immune Activation ◽  
Fetal Liver ◽  
Fetal Brain ◽  
Protein Translation ◽  
Maternal Immune Activation ◽  
Acute Response ◽  
Mouse Placenta ◽  
Trna Halves ◽  
Maternal Fetal Interface

AbstracttRNA-derived small fragments (tRFs) and tRNA halves have emerging functions in different biological pathways, such as regulating gene expression, protein translation, retrotransposon activity, transgenerational epigenetic changes and response to environmental stress. However, small RNAs like tRFs and microRNAs in the maternal-fetal interface during gestation have not been studied extensively. Here we investigated the small RNA composition of mouse placenta/decidua, which represents the interface where the mother communicates with the fetus, to determine whether there are specific differences in tRFs and microRNAs during fetal development and in response to maternal immune activation (MIA). Global tRF expression pattern, just like microRNAs, can distinguish tissue types among placenta/decidua, fetal brain and fetal liver. In particular, 5’ tRNA halves from tRNAGly, tRNAGlu, tRNAVal and tRNALys are abundantly expressed in the normal mouse placenta/decidua. Moreover, tRF and microRNA levels in the maternal-fetal-interface change dynamically over the course of embryonic development. To see if stress alters non-coding RNA expression at the maternal-fetal interface, we treated pregnant mice with a viral infection mimetic, which has been shown to promote autism-related phenotypes in the offspring. Acute changes in the levels of specific tRFs and microRNAs were observed 3-6 hours after MIA and are suppressed thereafter. A group of 5’ tRNA halves is down-regulated by MIA, whereas a group of 18-nucleotide tRF-3a is up-regulated. In conclusion, tRFs show tissue-specificity, developmental changes and acute response to environmental stress, opening the possibility of them having a role in the fetal response to MIA.

Maternal Immune Activation in the Rat Alters Maternofetal Leucine Transport and Fetal Brain Growth

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e13
Author(s):  
Hager M. Kowash ◽  
Harry G. Potter ◽  
Nick Ashton ◽  
Reinmar Hager ◽  
Joanna C. Neill ◽  
...  
Keyword(s):  
Immune Activation ◽  
Fetal Brain ◽  
Brain Growth ◽  
Maternal Immune Activation ◽  
Leucine Transport

Poster #10 EFFECTS OF MATERNAL IMMUNE ACTIVATION ON GENE EXPRESSION PATTERNS IN THE FETAL BRAIN

2012 ◽  
Vol 136 ◽  
pp. S188
Author(s):  
Krassimira A. Garbett ◽  
Elaine Y. Hsiao ◽  
Sara Kálmán ◽  
Paul H. Patterson ◽  
Károly Mirnics
Keyword(s):  
Gene Expression ◽  
Immune Activation ◽  
Expression Patterns ◽  
Fetal Brain ◽  
Gene Expression Patterns ◽  
Maternal Immune Activation

scholarly journals Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6

2007 ◽  
Vol 27 (40) ◽  
pp. 10695-10702 ◽  
Author(s):  
S. E. P. Smith ◽  
J. Li ◽  
K. Garbett ◽  
K. Mirnics ◽  
P. H. Patterson
Keyword(s):  
Brain Development ◽  
Immune Activation ◽  
Interleukin 6 ◽  
Fetal Brain ◽  
Maternal Immune Activation ◽  
Fetal Brain Development

scholarly journals Mycobacterium tuberculosis-Induced Maternal Immune Activation Promotes Autism-Like Phenotype in Infected Mice Offspring

2021 ◽  
Vol 18 (9) ◽  
pp. 4513
Author(s):  
Wadzanai Manjeese ◽  
Nontobeko E. Mvubu ◽  
Adrie J. C. Steyn ◽  
Thabisile Mpofana
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Immune Activation ◽  
Fetal Brain ◽  
Autism Spectrum ◽  
Necrosis Factor Alpha ◽  
Altered Expression ◽  
Maternal Immune Activation ◽  
Persistent Inflammation ◽  
Cytokine Levels ◽  
Fetal Brain Development

The maternal system’s exposure to pathogens during pregnancy influences fetal brain development causing a persistent inflammation characterized by elevated pro-inflammatory cytokine levels in offspring. Mycobacterium tuberculosis (Mtb) is a global pathogen that causes tuberculosis, a pandemic responsible for health and economic burdens. Although it is known that maternal infections increase the risk of autism spectrum disorder (ASD), it is not known whether Mtb infection is sufficient to induce ASD associated behaviors, immune dysregulation and altered expression of synaptic regulatory genes. The current study infected pregnant Balb/c mice with Mtb H37Rv and valproic acid (VPA) individually and in combination. Plasma cytokine profiles were measured in offspring using the Bio-plex Th17 pro mouse cytokine panel. Mtb infection increased plasma interleukin (IL)-6 and IL-17A, while tumor necrosis factor alpha (TNF-α), interferon (IFN)-γ and IL-1β were reduced when compared with saline. Mtb-induced maternal immune activation (MIA) offspring displayed increased grooming behavior. The study also revealed dysregulation in gene expression of synaptic molecules in the cerebellum. MIA rescued the VPA-induced effects on self-grooming and social interaction behaviors. Our finding therefore highlights a potential role of Mtb as a MIA agent that can potentially contribute to ASD.

scholarly journals Maternal immune activation in mice disrupts proteostasis in the fetal brain

2020 ◽  
Author(s):  
Brian T. Kalish ◽  
Eunha Kim ◽  
Benjamin Finander ◽  
Erin E. Duffy ◽  
Hyunju Kim ◽  
...  
Keyword(s):  
Immune Activation ◽  
Fetal Brain ◽  
Maternal Immune Activation

scholarly journals Maternal immune activation generates anxiety in offspring: A translational meta-analysis

BJPsych Open ◽  
2021 ◽  
Vol 7 (S1) ◽  
pp. S268-S268
Author(s):  
Ursula Matos ◽  
Laiana Azevedo Quagliato ◽  
Antonio Egidio Nardi
Keyword(s):  
Anxiety Disorders ◽  
Immune Activation ◽  
Synapse Formation ◽  
Meta Analysis ◽  
Fetal Brain ◽  
Cochrane Library ◽  
Future Research ◽  
Maternal Immune Activation ◽  
Genetic And Environmental Factors ◽  
And Function

AimsMaternal immune activation (MIA) during pregnancy is recognized as an etiological risk factor for various psychiatric disorders, such as schizophrenia, major depressive disorder, and autism. Prenatal immune challenge may serve as a “disease primer” into an altered trajectory of fetal brain development that, in combination with other genetic and environmental factors, may ultimately result in the emergence of different psychiatric conditions. However, the association between MIA and the offspring's chances of developing anxiety disorders is less clear. To examine the effect of MIA on offspring anxiety, a systematic review and meta-analysis of the preclinical literature was conducted.MethodA systematic search of the PubMed, Web of Science, PsycINFO, and Cochrane Library electronic databases was performed using the PRISMA and WHO methodologies for systematic reviews. Studies that investigated if MIA during rodent's pregnancy could cause anxiety symptoms in offspring were included.ResultOverall, the meta-analysis showed that MIA induced anxiety behavior in offspring. The studies provide strong evidence that prenatal immune activation impacts specific molecular targets, synapse formation and function, and a disbalance in neurotransmission that could be related to the generation of offspring anxiety. Future research should further explore the role of MIA in anxiety endophenotypes.ConclusionAccording to this meta-analysis, MIA plays an important role in the pathophysiological mechanisms of anxiety disorders and provides a promising therapeutic target.

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