Estrogen Receptor β as a Candidate Regulator of Sex Differences in the Maternal Immune Activation Model of ASD

Interestingly, more males are diagnosed with autism spectrum disorder (ASD) than females, yet the mechanism behind this difference is unclear. Genes on the sex chromosomes and differential regulation by sex steroid hormones and their receptors are both candidate mechanisms to explain this sex-depend...

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Bibliographic Details
Published in:Frontiers in molecular neuroscience 2021-08, Vol.14, p.717411-717411
Main Authors: Arnold, Madeline L., Saijo, Kaoru
Format: Article
Language:English
Subjects:
Autism
autism spectrum disorder
Brain
brain myeloid cells
Cytokines
estrogen receptor β
Estrogen receptors
Estrogens
Etiology
Females
Gender differences
Gene expression
Hormones
Immune response
Inflammation
Ligands
Males
maternal immune activation
Molecular Neuroscience
Neurodevelopmental disorders
Nuclear receptors
Phenotypes
Sex chromosomes
Sex differences
Sex hormones
Steroid hormones
Steroids
Stimulants
Transcription factors
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Summary:Interestingly, more males are diagnosed with autism spectrum disorder (ASD) than females, yet the mechanism behind this difference is unclear. Genes on the sex chromosomes and differential regulation by sex steroid hormones and their receptors are both candidate mechanisms to explain this sex-dependent phenotype. Nuclear receptors (NRs) are a large family of transcription factors, including sex hormone receptors, that mediate ligand-dependent transcription and may play key roles in sex-specific regulation of immunity and brain development. Infection during pregnancy is known to increase the probability of developing ASD in humans, and a mouse model of maternal immune activation (MIA), which is induced by injecting innate immune stimulants into pregnant wild-type mice, is commonly used to study ASD. Since this model successfully recaptures the behavioral phenotypes and male bias observed in ASD, we will discuss the potential role of sex steroid hormones and their receptors, especially focusing on estrogen receptor (ER)β, in MIA and how this signaling may modulate transcription and subsequent inflammation in myeloid-lineage cells to contribute to the etiology of this neurodevelopmental disorder.
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2021.717411