Evidence map›Paper›PMID 36803626›Full record

ArticleBiology of sex differences2023

Investigation of autism-related transcription factors underlying sex differences in the effects of bisphenol A on transcriptome profiles and synaptogenesis in the offspring hippocampus.

Surangrat Thongkorn, Songphon Kanlayaprasit, Kasidit Kasitipradit, Pattanachat Lertpeerapan, Pawinee Panjabud, Valerie W Hu, Depicha Jindatip, Tewarit Sarachana

Open access · goldAbstract read
In one paragraph

Article in Biology of sex differences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 28 citations in OpenAlex.

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  20. The Autism Spectrum Disorder and Its Possible Origins in Pregnancy.International journal of environmental research and public health · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Surangrat ThongkornDepartment of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Songphon KanlayaprasitSYstems Neuroscience of Autism and PSychiatric Disorders (SYNAPS) Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, 154 Soi Chula 12, Rama 1 Road, Wangmai, Pathumwan, Bangkok, 10330, Thailand.
Kasidit KasitipraditDepartment of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Pattanachat LertpeerapanDepartment of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Pawinee PanjabudDepartment of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand.
Valerie W HuDepartment of Biochemistry and Molecular Medicine, The George Washington University School of Medicine and Health Sciences, The George Washington University, Washington, DC, USA.
Depicha JindatipSYstems Neuroscience of Autism and PSychiatric Disorders (SYNAPS) Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, 154 Soi Chula 12, Rama 1 Road, Wangmai, Pathumwan, Bangkok, 10330, Thailand.
Tewarit SarachanaSYstems Neuroscience of Autism and PSychiatric Disorders (SYNAPS) Research Unit, Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, 154 Soi Chula 12, Rama 1 Road, Wangmai, Pathumwan, Bangkok, 10330, Thailand. tewarit.sa@chula.ac.th.ORCID 0000-0003-4518-9399
Chulalongkorn University · THGeorge Washington University · US

Funding

Chulalongkorn University GCUGR1125632108D-108Chulalongkorn University GCUGR1125632109D-109Chulalongkorn University GCUGR1125651060D-060Chulalongkorn University GCUGR1125651062D-062Chulalongkorn University GRU 6300437001-1Chulalongkorn University GRU_64_033_37_004Chulalongkorn University GRU 6506537004-1Chulalongkorn University HEA663700091National Research Council of Thailand PHD/0029/2561Office of the Higher Education Commission NRU59-031-HR
6 · The paper itself

Abstract

backgroundBisphenol A (BPA) has been linked to susceptibility to autism spectrum disorder (ASD). Our recent studies have shown that prenatal BPA exposure disrupted ASD-related gene expression in the hippocampus, neurological functions, and behaviors associated with ASD in a sex-specific pattern. However, the molecular mechanisms underlying the effects of BPA are still unclear.

methodsTranscriptome data mining and molecular docking analyses were performed to identify ASD-related transcription factors (TFs) and their target genes underlying the sex-specific effects of prenatal BPA exposure. Gene ontology analysis was conducted to predict biological functions associated with these genes. The expression levels of ASD-related TFs and targets in the hippocampus of rat pups prenatally exposed to BPA were measured using qRT-PCR analysis. The role of the androgen receptor (AR) in BPA-mediated regulation of ASD candidate genes was investigated using a human neuronal cell line stably transfected with AR-expression or control plasmid. Synaptogenesis, which is a function associated with genes transcriptionally regulated by ASD-related TFs, was assessed using primary hippocampal neurons isolated from male and female rat pups prenatally exposed to BPA.

resultsWe found that there was a sex difference in ASD-related TFs underlying the effects of prenatal BPA exposure on the transcriptome profiles of the offspring hippocampus. In addition to the known BPA targets AR and ESR1, BPA could directly interact with novel targets (i.e., KDM5B, SMAD4, and TCF7L2). The targets of these TFs were also associated with ASD. Prenatal BPA exposure disrupted the expression of ASD-related TFs and targets in the offspring hippocampus in a sex-dependent manner. Moreover, AR was involved in the BPA-mediated dysregulation of AUTS2, KMT2C, and SMARCC2. Prenatal BPA exposure altered synaptogenesis by increasing synaptic protein levels in males but not in females, but the number of excitatory synapses was increased in female primary neurons only.

conclusionsOur findings suggest that AR and other ASD-related TFs are involved in sex differences in the effects of prenatal BPA exposure on transcriptome profiles and synaptogenesis in the offspring hippocampus. These TFs may play an essential role in an increased ASD susceptibility associated with endocrine-disrupting chemicals, particularly BPA, and the male bias of ASD.

Indexed as

Autism Spectrum DisorderAutistic DisorderAnimalsBisphenol A CompoundsDNA-Binding ProteinsFemaleHippocampusHumansMaleMolecular Docking SimulationPregnancyRatsSex CharacteristicsTranscription FactorsTranscriptomebisphenol ABisphenol A CompoundsDNA-Binding ProteinsSMARCC2 protein, humanTranscription FactorsAndrogen receptorAutism spectrum disorderBisphenol AEndocrine-disrupting chemicalMicroplasticsMolecular dockingSex differenceSynaptogenesisTranscription factor

Identifiers

PMID36803626
PMCPMC9940328
OpenAlexW4321371516

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.