Macaca fascicularis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391415 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5739550_1.fastq.gz | Fastqsanger.gz | |||
| SRR5739550_2.fastq.gz | Fastqsanger.gz | |||
| SRR5739551_1.fastq.gz | Fastqsanger.gz | |||
| SRR5739551_2.fastq.gz | Fastqsanger.gz | |||
| SRR5739522_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:Valproic acid (VPA) is a clinically used antiepileptic drug, but it has significant risks for low verbal intelligence quotient scores, attention deficit hyperactivity disorder and autism spectrum disorder in children when it is administered during pregnancy. Prenatal VPA exposure is reported to affect neurogenesis and neuronal migration and differentiation. In addition, growing evidence showed that a brain immune cell, microglia are activated by VPA treatment. However, a role of activated microglia by VPA remains unclear. The purpose of this study is identify a candidate gene which is responsible for VPA-induced behavioral disorders.
2021-07-23 | GSE180564 | GEO
Project description:Autism spectrum disorders (ASDs) are a neurodevelopmental disorder characterized by impairments in social interactions and stereotyped behaviors. While ASD has a strong genetic background, environmental factors including toxins, pesticides, infection and drugs are also known to confer autism susceptibility, likely by inducing epigenetic changes. Exposure to Valproic acid (VPA), a drug for epilepsy and bipolar disorders, during pregnancy is highly associated with the risk of ASD children. In rodents, in utero VPA exposure can precipitate behavioral phenotypes related to ASD in the offspring. Since VPA is an inhibitor of histone deacethytransferase (HDAC) activity, it thought to cause ASD with epigenetic modification. However, the core mechanism by which prenatal VPA exposure causes onset of ASD is still not fully uncovered. Here we revealed that prenatal VPA exposure strongly influences development of vasoactive intestinal peptide (VIP) - positive neurons, a subtype of cortical GABAergic interneurons. The number of VIP+ interneurons was severely reduced in somatosensory area of VPA-exposed ASD animals. We then found that the reduction in VIP+ interneurons is caused by the inhibition of HDAC3 activity upon prenatal VPA exposure. Importantly, prenatal HDAC3 inhibition caused not only the selective reduction in VIP+ interneurons but also the ASD-like behaviors in mice. We then demonstrated that the HDAC3 inhibition aberrantly activates Notch signaling, which influences the cell fate determination of VIP+ interneuron progenitors in caudal ganglionic eminence. Thus, this study uncovers the mechanism by which specific HDAC inhibition during development influences a specific type of GABAergic interneurons in the ASD model. The findings provide a novel insight into the understanding of ASD pathophysiology.
2022-06-20 | GSE133932 | GEO
Project description:Autism spectrum disorder (ASD) affects gene expression in adult ages. We used valproic acid (VPA)-induced ASD model marmosets. Gene expression modulations in VPA-exposed and unexposed (UE) marmosets were analyzed at adult ages. We revealed modulations in neuron- and glia-related genes.
2022-05-01 | GSE199560 | GEO
Project description:Autism spectrum disorder (ASD) affects gene expression in early postnatal development. We used valproic acid (VPA)-induced ASD model marmosets. Gene expression in VPA-exposed and unexposed (UE) marmosets were analyzed at 0, 3 and 6 months (M). We revealed three groups of differentially expressed genes based on the temporal patterns of modulation.
2021-04-01 | GSE156186 | GEO
Project description:Autism Spectrum Disorder (ASD) is a developmental disorder characterized by impaired social communication and repetitive behaviors. In recent years, a pharmacological mouse model of ASD involving maternal administration of valproic acid (VPA) has become widely used. Newborn pups in this model show an abnormal balance between excitatory and inhibitory (E/I) signaling in neurons and exhibit ASD-like behavior. To elucidate the molecular basis of this model, we analyzed secretome of primary neurons cultured from embryos maternally treated with or without VPA.
2024-10-26 | PXD042099 | JPOST Repository
Project description:Prenatal exposure to the anti-seizure drug sodium valproate (VPA) is associated with an increased risk of adverse postnatal neurodevelopmental outcomes, including lowered intellectual ability, autism spectrum disorder and attention-deficit hyperactivity disorder. In this study, we aimed to clarify the molecular mechanisms underpinning the neurodevelopmental consequences of gestational VPA exposure using integrative genomics. First, we assessed the effect of gestational VPA on fetal brain gene expression using a validated rat model of valproate teratogenicity that mimics the human scenario of chronic oral valproate treatment during pregnancy at doses which are therapeutically relevant to the treatment of epilepsy. Two different rat strains were studied - inbred Genetic Absence Epilepsy Rats from Strasbourg (GAERS), a model of genetic generalized epilepsy, and inbred Non-Epileptic Control (NEC) rats. Female rats were fed standard chow or VPA mixed in standard chow for 2 weeks prior to conception and then mated with same-strain males. In the VPA-exposed rats maternal oral treatment was continued throughout pregnancy. Fetuses were extracted via C-section on gestational day 21 (one day prior to birth) and fetal brains were snap frozen and genome-wide gene expression data generated. We found that gestational VPA exposure via chronic maternal oral dosing was associated with substantial drug-induced differential gene expression in the pup brains, including dysregulated splicing, and observed that this occurred in the absence of evidence for significant neuronal gain or loss. The set of genes down-regulated by VPA in the pup brains were significantly enriched for pathways related to neurodevelopment and synaptic function, and significantly enriched for heritability to human intelligence, schizophrenia and bipolar disorder. Our results provide a mechanistic link between chronic fetal VPA exposure and adverse neurodevelopmental outcomes mediated by VPA-induced transcriptional dysregulation.
2022-05-08 | GSE198756 | GEO
Project description:PsychENCODE Consortium: Epigenetic Dysregulation in Autism Spectrum Disorder
| PRJNA344520 | ENA
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.
2023-11-04 | GSE246534 | GEO
Project description:In this study, we explored molecular alterations in the hippocampus of prenatal valproic acid (VPA)-exposed rats as a model of autism spectrum disorders (ASD). In addition, we assessed effects of chronic administration of intranasal oxytocin, a promising peptide for ASD treatment. Comparative analyses revealed that prenatal VPA exposure altered gene expression, a part of which is involved in key features including memory, developmental process, and epilepsy. Oxytocin partly improved these gene expression, which were predicted to interact with those involved in social behaviors and hippocampal-dependent memory. The present study documented molecular profiling in the hippocampus related to ASD and improvement by chronic treatment of oxytocin.
2022-02-12 | GSE196500 | GEO
Project description:Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental disorder where patients have impaired social behavior, communication, repetitive behaviors, and restricted interest. Valproic acid (VPA) has been widely used to treat patients with epilepsy and bipolar disorder patients. However, VPA treatment during pregnancy has produced offspring with neurodevelopmental disorders, including ASD. To better understand the molecular function of ASD, we have used valproic acid, chemically induced ASD mice. We have performed LC-MS/MS analysis of VPA-induced offspring mice to the control to see the difference in their proteome difference. Our analysis showed that many neuronal network pathways were highly expressed in our differentially expressed proteins, and among them, Wnt/ β-catenin pathways showed clear enrichment. The RNF146 (E3 Ubiquitin-protein ligase) increase in VPA-exposed mice showed a highly significant effect on canonical Wnt/ β-catenin signaling pathways by disrupting the β-catenin destruction complex. The proteins like CREBBP, TCF4, and GSK3B also showed significant changes that indicate dysfunction of β-catenin destruction complex and activation of transcription factors.
2023-07-24 | PXD036413 | Pride