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Implications of Prenatal Exposure to Hyperandrogen for Hippocampal Neurodevelopment and Autism-like Behavior in Offspring

ABSTRACT: Implications of Prenatal Exposure to Hyperandrogen for Hippocampal Neurodevelopment and Autism-like Behavior in Offspring

PROVIDER: PRJNA1033587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26590006_1.fastq.gz	Fastqsanger.gz
	SRR26590006_2.fastq.gz	Fastqsanger.gz
	SRR26590007_1.fastq.gz	Fastqsanger.gz
	SRR26590007_2.fastq.gz	Fastqsanger.gz
	SRR26590008_1.fastq.gz	Fastqsanger.gz

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Implications of Prenatal Exposure to Hyperandrogen for Hippocampal Neurodevelopment and Autism-like Behavior in Offspring

Project description:Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental disorder that significantly jeopardizes the physical and mental well-being of children. Autism spectrum disorder results from a combination of environmental and genetic factors. Hyperandrogenic exposure during pregnancy increases their risk of developing autism. Nevertheless, the prenatal exposure to androgens affects offspring neurodevelopment and the underlying mechanisms have not been fully elucidated. In the present study, administration of excessive dihydrotestosterone (DHT) to pregnant mice was found to impair neuronal development and dendritic spine formation in offspring, inducing autism-like behaviors. Furthermore, through mRNA transcriptome sequencing technology, the key molecule Nr4a2 was identified during this process of change. Overexpression of Nr4a2 and treatment with amodiaquine (AQ) significantly improved the abnormal phenotypes in offspring caused by prenatal exposure to androgens. Overall, Nr4a2 emerges as a crucial molecule involved in the impairment of offspring neurodevelopment due to prenatal androgen exposure, which provides a new perspective for the in-depth study of the influencing factors and underlying mechanisms.

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The chromatin modifier CHD8 targets autism risk genes during human neurodevelopment

Project description:Whole-exome sequencing studies have implicated chromatin modifiers and transcriptional regulators in autism spectrum disorder (ASD) through the identification of de novo loss of function mutations in affected individuals. Many of these genes are co-expressed in mid-fetal human cortex, suggesting ASD risk genes converge in regulatory networks that are perturbed in ASD during neurodevelopment. To elucidate such networks we mapped promoters and enhancers bound by the chromodomain helicase CHD8, which is strongly enriched in ASD-associated de novo loss of function mutations, using ChIP-seq in mid-fetal human brain, human neural stem cells (hNSCs), and embryonic mouse cortex. We find that CHD8 targets are strongly enriched for ASD risk genes that converge in ASD-associated co-expression networks in human midfetal cortex. CHD8 knockdown in hNSCs results in significant dysregulation of ASD risk genes targeted by CHD8, as well as additional genes important for neurodevelopment, including members of the Wnt/β-catenin signaling pathway. Integration of CHD8 binding data with genetic and gene co-expression data in ASD risk models provides support for additional ASD risk genes. Together, our results suggest that loss of CHD8 function contributes to ASD through regulatory perturbation of other ASD risk genes during human cortical development.

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Project description:The prenatal period is a critical window to study factors involved in the development of autism spectrum disorder (ASD). Environmental factors, especially in utero nutrition, can interact with genetic risk for ASD, but how specific prenatal nutrients in mothers of children later diagnosed with ASD or non-typical development (Non-TD) associate with gestational gene expression events is poorly understood. Maternal blood collected prospectively during pregnancy provides a new opportunity to gain insights into nutritional effects on gene pathways and neurodevelopment. Using differential gene expression analysis, six transcripts associated with four genes (TGR-AS1, SQSTM1, HLA-C and RFESD) showed genome-wide significance (FDR q < 0.05) with child outcomes. Genes nominally differentially expressed compared to TD (p < 0.05) specifically in ASD, but not Non-TD, significantly overlapped with seven high confidence ASD genes. 218 transcripts in common to ASD and Non-TD differential expression compared to TD were significantly enriched for functions in immune response to interferon-gamma, apoptosis, and metal ion transport. WGCNA identified co-expressed gene modules significantly correlated with 5-MeTHF, folic acid, DMG and betaine. A module enriched in DNA methylation functions showed a protective association with folic acid/5-MeTHF concentrations and ASD risk. Independent of child outcome, maternal plasma betaine and DMG concentrations associated with a block of co-expressed genes enriched for adaptive immune, histone modification, and RNA processing functions. These results support the premise that the prenatal maternal blood transcriptome is a sensitive indicator of gestational nutrition and children’s later neurodevelopmental outcomes.

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Project description:In this study, we investigated the effects of prenatal bisphenol-A (BPA) exposure on transcriptome profiles in the frontal cortex of the rat offspring. Transcriptome profiling by RNA-seq analysis of frontal cortex tissues isolated from neonatal pups prenatally exposed to BPA revealed that a list of differentially expressed genes (DEGs) associated with autism spectrum disorder (ASD), including Ntng1, Auts2, and Ankrd11 was dysregulated in a sex-specific pattern. The gene ontology analysis revealed that the BPA-responsive genes in the offspring’s frontal cortex were significantly associated with ASD-related neurological functions. These results indicated that prenatal BPA exposure may increase the risk of ASD by impacting ASD-related genes in the offspring’s frontal cortex. We conducted experiments using the frontal cortex from neonatal pups prenatally exposed to BPA or vehicle control (BPA treament; pooled 3 pups frontal cortex, vehicle control; pooled 3 pups frontal cortex). 10-week-old female rats were daily treated with BPA at the concentration of 5,000 microgram/kilogram of maternal body weight or vehicle control from gestation day 1 (GD1) until parturition. Total RNAs were isolated and cDNAs were synthesized. The transcriptome profiles were performed using a high-throughtput RNA-seq.

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Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology.

Project description:We investigate the role of the mitochondrion, an organelle highly sensitive to environmental agents, in the influence of prenatal air pollution exposure on neurodevelopment and behavior in 96 children with autism spectrum disorder (ASD) [45 with neurodevelopmental regression (NDR); 76% Male; mean (SD) age 10 y 9 m (3 y 9 m)]. Mitochondrial function was assessed using the Seahorse XFe96 in fresh peripheral blood mononuclear cells. Second and third trimester average and maximal daily exposure to fine air particulate matter of diameter ≤2.5 µm (PM2.5) was obtained from the Environmental Protection Agency's Air Quality System. Neurodevelopment was measured using the Vineland Adaptive Behavior Scale 2nd edition and behavior was assessed using the Aberrant Behavior Checklist and Social Responsiveness Scale. Prenatal PM2.5 exposure influenced mitochondrial respiration during childhood, but this relationship was different for those with (r = 0.25-0.40) and without (r = -0.07 to -0.19) NDR. Mediation analysis found that mitochondrial respiration linked to energy production accounted for 25% (SD = 2%) and 10% (SD = 2%) of the effect of average prenatal PM2.5 exposure on neurodevelopment and behavioral symptoms, respectively. Structural equation models estimated that PM2.5 and mitochondrial respiration accounted for 34% (SD = 4%) and 36% (SD = 3%) of the effect on neurodevelopment, respectively, and that behavior was indirectly influenced by mitochondrial respiration through neurodevelopment but directly influenced by prenatal PM2.5. Our results suggest that prenatal exposure to PM2.5 disrupts neurodevelopment and behavior through complex mechanisms, including long-term changes in mitochondrial respiration and that patterns of early development need to be considered when studying the influence of environmental agents on neurodevelopmental outcomes.

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