Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fetal Growth Restriction Impairs Hippocampal Neurogenesis and Cognition via Tet1 in Offspring

ABSTRACT: Fetal Growth Restriction Impairs Hippocampal Neurogenesis and Cognition via Tet1 in Offspring

PROVIDER: PRJNA601762 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15222939_1.fastq.gz	Fastqsanger.gz
	SRR15222939_2.fastq.gz	Fastqsanger.gz
	SRR15222940_1.fastq.gz	Fastqsanger.gz
	SRR15222940_2.fastq.gz	Fastqsanger.gz
	SRR15222941_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Fetal Growth Restriction Impairs Hippocampal Neurogenesis and Cognition via Tet1 in Offspring

Project description:Fetal growth restriction (FGR) increases the risk for impaired cognitive function later in life. However, the precise mechanisms remain elusive. Using dexamethasone-induced FGR and protein restriction-influenced FGR mouse models, we observed learning and memory deficits in adult FGR offspring. FGR induces decreased hippocampal neurogenesis from the early postnatal period to adulthood by reducing the proliferation of neural stem cells (NSCs). We further found a persistent decrease of Tet1 expression in hippocampal NSCs of FGR mice. Mechanistically, Tet1 downregulation results in hypermethylation of the Dll3 and Notch1 promoters and inhibition of Notch signaling, leading to reduced NSC proliferation. Overexpression of Tet1 activates Notch signaling, offsets the decline in neurogenesis, and enhances learning and memory abilities in FGR offspring. Our data indicate that a long-term decrease in Tet1/Notch signaling in hippocampal NSCs contributes to impaired neurogenesis following FGR and could serve as potential targets for the intervention of FGR-related cognitive disorders.

2021-09-15 | GSE143816 | GEO

Tet1 regulates adult hippocampal neurogenesis and cognition.

Project description:DNA hydroxylation catalyzed by Tet dioxygenases occurs abundantly in embryonic stem cells and neurons in mammals. However, its biological function in vivo is largely unknown. Here, we demonstrate that Tet1 plays an important role in regulating neural progenitor cell proliferation in adult mouse brain. Mice lacking Tet1 exhibit impaired hippocampal neurogenesis accompanied by poor learning and memory. In adult neural progenitor cells deficient in Tet1, a cohort of genes involved in progenitor proliferation were hypermethylated and downregulated. Our results indicate that Tet1 is positively involved in the epigenetic regulation of neural progenitor cell proliferation in the adult brain.

| S-EPMC4474382 | biostudies-literature

Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

Project description:Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

| PRJNA688636 | ENA

m6A modification involves in enriched environment-induced neurogenesis and cognition enhancement

Project description:m6A modification involves in enriched environment-induced neurogenesis and cognition enhancement

| PRJNA811978 | ENA

Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

Project description:Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

| PRJNA694166 | ENA

Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1

Project description:Using RNA sequencing, we found that Tet1 alters gene expression. Mechanistically, we found that Tet1 deficiency leads to the abnormal Ca2+ signaling by regulating the expression of GluA1, which can be rescued by ectectopic expression of GluA1. Collectively, our findings suggest that Tet1 plays important functions by regulating astrocytes Ca2+ signaling.

2021-11-17 | GSE164025 | GEO

Disrupted de novo pyrimidine biosynthesis impairs adult hippocampal neurogenesis and cognition in pyridoxine-dependent epilepsy.

Project description:Despite seizure control by early high-dose pyridoxine (vitamin B6) treatment, at least 75% of pyridoxine-dependent epilepsy (PDE) patients with ALDH7A1 mutation still suffer from intellectual disability. It points to a need for additional therapeutic interventions for PDE beyond pyridoxine treatment, which provokes us to investigate the mechanisms underlying the impairment of brain hemostasis by ALDH7A1 deficiency. In this study, we show that ALDH7A1-deficient mice with seizure control exhibit altered adult hippocampal neurogenesis and impaired cognitive functions. Mechanistically, ALDH7A1 deficiency leads to the accumulation of toxic lysine catabolism intermediates, α-aminoadipic-δ-semialdehyde and its cyclic form, δ-1-piperideine-6-carboxylate, which in turn impair de novo pyrimidine biosynthesis and inhibit NSC proliferation and differentiation. Notably, supplementation of pyrimidines rescues abnormal neurogenesis and cognitive impairment in ALDH7A1-deficient adult mice. Therefore, our findings not only define the important role of ALDH7A1 in the regulation of adult hippocampal neurogenesis but also provide a potential therapeutic intervention to ameliorate the defective mental capacities in PDE patients with seizure control.

| S-EPMC10997211 | biostudies-literature

Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis

Project description:Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis

| PRJNA590654 | ENA

Astrocytes Tet1 regulates neuronal development and cognition through modulating GluA1 in mice

Project description:Tet (Ten eleven translocation) mediated 5-hydroxymethylcytosine (5hmC) is highly enriched in the neuronal system and is involved in diverse biological processes and diseases. However, the function of 5hmC in astrocytes remains completely unknown. In the present study, we show that Tet1 deficiency alters astrocytes morphology and impairs neuronal function. Specific deletion of Tet1 in astrocytes impairs learning and memory ability of mice. Using 5hmC high-throughput DNA sequencing and RNA sequencing, we found the distribution feature of 5hmC in astrocytes and that Tet1 deficiency induces DNA hydroxymethylation regions (DhMRs) and alters gene expression. Mechanistically, we found that Tet1 deficiency leads to the abnormal Ca2+ signaling by regulating the expression of GluA1, which can be rescued by ectectopic expression of GluA1. Collectively, our findings suggest that Tet1 plays important functions by regulating astrocytes Ca2+ signaling.

2021-11-17 | GSE165370 | GEO

Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis [hADSCs]

Project description:Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis [hADSCs]

| PRJNA590665 | ENA