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MeDIP-Chip from deliveries of control fetuses or fetuses with NTDs

ABSTRACT: Neural-tube defects (NTDs) are common birth defects of complex etiology. Although many studies have confirmed a genetic component, the exact mechanism between DNA methylation and NTDs remains unclear.In this study,the alteration of methylation from placental tissues of normal infants or with NTDs.Results demonstrated that DNA methylation changed in specific gene location.

ORGANISM(S): Homo sapiens

PROVIDER: GSE87319 | GEO | 2016/09/24

SECONDARY ACCESSION(S): PRJNA344337

REPOSITORIES: GEO

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Single-nuclus sequencing analysis reveals aberrant brain development in fetuses with neural tube defects

Project description:Background: Neural tube defects (NTDs) are congenital malformations that occur when the neural tube fails to close properly during early embryonic development. However, the identity of affected celltypes and pathogenic mechanisms remain unclear due to the lack of clinical samples. Method: We utilized single-nucleus RNA sequencing to analyze 37,064 neural tube cells from NTDs and normal abortus at 14 and 15 gestational weeks. Multiplexed immunofluorescence staining was performed to further validate some phenotypes. Results: Firstly, we revealed that the most affected celltypes are excitatory neurons, inhibitory neurons, and astrocytes. We further elucidated that the main subtypes mediating abnormal development in NTDs is IGF2high subtypes in inhibitory neurons and MEG3high subtypes in astrocytes. Importantly, our findings highlighted IGF2 as a pivotal gene for abnormal development and abnormal cell-cell communications in NTDs. Conclusions: In summary, this study presents the first single-cell atlas of NTDs and provides new insights for further research into the underlying mechanisms of NTDs.

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Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [MeDIP]

Project description:To investigate the associated with abnormal DNA demethylation and neural tube defects (NTDs) with folate deficiency, we etablished mouse embryonic stem cells (mESCs) Sv/129 in folate-deficiency-treated.

2022-09-20 | GSE204872 | GEO

mRNA expression profiles of Neural Tube Defects (NTDs) in the 2nd trimester of human fetus

Project description:Neural Tube Defects (NTDs) are serious health problems of infants, accounting for large proportion of live birth defects in infants and miscarriage in women worldwide. Although some epidemiologic studies suggest both genetic and environmental factors were involved in the progression of the diseases, the etiologies of NTDs are not well understood at present. The objective of our study was to generate and to compare mRNA profiles of NTDs with those of normal controls in the 2nd trimesters of pregnancy. Illumina microarray chips (beadarrays) were utilized to identify the altered mRNA transcripts in the organ samples recruited from Luliang Prefecture in Shanxi Province, China, which has the highest occurrence of NTDs in world. The beadarrays identified 101 un-regulated and 194 down-regulated mRNA transcripts in the NTDs compared with the controls in the spinal cord. A number of genes in the cholesterol biosynthesis pathway were down-regulated. In particular, SIRT2, a key regulator of cholesterol biosynthesis, was significantly down-regulated in NTD samples. Our findings provide evidences that, the decrease of cholesterol biosynthesis in the spinal cord of NTD may affect the neural tube closure in the affected fetuses.

2019-10-10 | GSE33111 | GEO

Profiling placental and fetal DNA methylation in human neural tube defects

Project description:The incidence of neural tube defects (NTDs) declined by about 40% in Canada with the introduction of national folic acid (FA) fortification programs. However, NTDs persist despite the fact that few Canadians currently exhibit folate deficiency. FA fortification may have aided in reducing NTDs by overcoming abnormal one carbon metabolism cycling, the process which provides one carbon units for methylation of DNA. We considered that NTDs persisting in a folate replete population may also occur in the context of compromised one carbon metabolism, and that this might manifest as abnormal DNA methylation (DNAm). Second trimester human placental chorionic villi, kidney, spinal cord, brain and muscle were collected from 19 control, 22 spina bifida and 15 anencephaly fetuses in British Columbia, Canada. DNA was extracted, assessed for methylenetetrahydrofolate reductase (MTHFR) genotype and for genome-wide DNAm using repetitive elements, in addition to the Illumina Infinium HumanMethylation450 (450k) array. No difference in repetitive element DNAm was noted. Using a false discovery rate <0.05 and average group difference in DNAm >0.05, differentially methylated array sites were only identified in (i) the comparison of anencephaly to controls in chorionic villi (n=4 sites) and (ii) the comparison of spina bifida to controls in kidney (n=3,342 sites). We suggest that the distinctive DNAm of spina bifida kidneys may be consequent to the neural tube defect. Although other studies have provided data to support altered DNAm in NTDs, this was not a major feature of British Columbian cases on a genome-wide or site specific level.

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RNA-seq profiling of neural tissue from mouse embryos with combined loss of p53 and Bim

Project description:Neural tube defects (NTDs) are common birth defects in humans and show an unexplained female bias. Female mice lacking the tumor suppressor p53 display NTDs with incomplete penetrance. We found that the combined loss of pro-apoptotic BIM and p53 caused 100% penetrant, female-exclusive NTDs, which allowed us to investigate the female-specific functions of p53. We report that female p53–/– neural tube samples show fewer cells with inactive X markers Xist and H3K27me3, and a concomitant increase in biallelic expression of the X-linked genes, Huwe1 and Usp9x. The depletion of Xist and increase X-linked gene expression was confirmed by RNA sequencing.

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Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [ChIP-seq]

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2022-09-20 | GSE204869 | GEO

DNA Methylation and Transcriptomic Profiles of Early Organogenesis-Stage Mouse Conceptuses after Exposure to Mono-2-Ethylhexyl Phthalate: Effects in the Absence and Presence of Neural Tube Defects

Project description:The goal of this study was to assess changes in gene expression and DNA methylation in response to embryonic exposures to the plasticizer metabolite, mono-2-ethylhexyl phthalate (MEHP). Because we previously observed increased incidence of neural tube defects (NTDs) in exposed embryos, we also stratified our samples by NTD status to examine changes in expression or methylation that may be associated with NTD progression in response to MEHP.

2024-07-31 | GSE180254 | GEO

Abnormal Transcriptome-wide of DNA demethylation in Folate deficiency caused neural tube defects [hMeDIP]

2022-09-20 | GSE204870 | GEO

Genes expression of WT and KLF12 overexpression mouse fetues at 9.0 dpc

Project description:Background: Although adequate periconceptional folic acid (FA) supplementation has reduced the occurrence of neural tube defects (NTDs)-affected pregnancies, mechanisms underlie FA resistant NTDs are poorly understood, so that NTDs still remain a global public health concern now. It has been proven that high level of Krüppel-like factor 12 (KLF12) has bad effects on heath in most cases, but there is no evidence concerning its roles during development. Methods: We used KLF12-overexpression mice to study the effects of high level of KLF12 on neural tube development. Findings: We showed KLF12-overexpression fetuses died in utero at around 10.5 days post coitus with 100% cranial NTDs. Neither FA or formate benefited normal neural tube closure in mutant fetuses. Further anylasis revealed high level of KLF12 caused NTDs in mice via overactivating Sonic hedgehog (Shh) signaling pathway, leading to upregulation of Ptch1, Gli1, Hhip etc. PF-5274857, an antagonist of Shh signaling pathway could significantly promote dorsolateral hinge point formation and partially rescue the phynotype. Interpretation: The regulatory hierarchy between high level of KLF12 and FA-resistant NTDs might provide new insights for the diagnosis and treatment of unexplained NTDs in the future.

2021-02-04 | GSE166054 | GEO

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Project description:Neural tube defects (NTDs) are one of the most common human birth defects, with a prevalence of approximately 1 in 1000 live births in the United States. In animal studies, deletion of p53 and hyperthermia leads to a significant increase in embryos that exhibit exencephaly. To evaluate the effects of hyperthermia on p53-deficient mouse embryos we used microarray approach to find genes modified by deletion of p53 and hyperthermia treatment in day 8.5 mouse embryos to identify genes that may be involved in the mechanisms underlining NTDs and begin to define the developmental role of p53 in the etiology of NTDs.

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