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MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE225102 | GEO | 2023/02/16

REPOSITORIES: GEO

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MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [RNA-Seq]

Project description:Epilepsy is considered to result from an imbalance between excitation and inhibition of the central nervous system. Pathogenic mutations in the methyl-CpG binding domain protein 5 gene (MBD5) are known to cause epilepsy. However, the function and mechanism of MBD5 in epilepsy remain elusive. Here, we found that MBD5 was mainly localized in the pyramidal cells and granular cells of mouse hippocampus, and its expression was increased in the brain tissues of mouse models of epilepsy. Exogenous overexpression of MBD5 inhibited the transcription of the signal transducer and activator of transcription 1 gene (Stat1), resulting in increased expression of N-methyl-D-aspartate receptor (NMDAR) subunit 1 (GluN1), 2A (GluN2A) and 2B (GluN2B), leading to aggravation of the epileptic behaviour phenotype in mice. In contrast, overexpression of STAT1 reduced the expression of NMDARs and alleviated the epileptic behavioural phenotype of mice. Furthermore, the epileptic behavioural phenotype was relieved by the NMDAR antagonist memantine. These results indicate that MBD5 accumulation affects seizures through STAT1-mediated inhibition of NMDAR expression in mice. Collectively, our findings suggest that the MBD5-STAT1- NMDAR pathway may be a new pathway that regulates the epileptic behavioural phenotype and may represent a new treatment target.

2023-02-16 | GSE225101 | GEO

MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [ChIP-Seq]

2023-02-16 | GSE225100 | GEO

MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription

Project description:MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription

| PRJNA933923 | ENA

MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [RNA-Seq]

Project description:MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [RNA-Seq]

| PRJNA934468 | ENA

MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [ChIP-Seq]

Project description:MBD5 regulates NMDA receptor expression and seizures by inhibiting Stat1 transcription [ChIP-Seq]

| PRJNA934463 | ENA

GLP-1 directed NMDA receptor antagonism for obesity treatment

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-14 | GSE245728 | GEO

UHRF2 regulates local 5-methylcytosine and suppresses spontaneous seizures

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-07-21 | GSE98362 | GEO

The SRSF4/lncRNA GAS5 axis regulates left ventricular hypertrophy by inhibiting the glucocorticoid receptor

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-08 | GSE131145 | GEO

RPAP2 regulates a transcription initiation checkpoint by inhibiting assembly of pre-initiation complex

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-03 | GSE193680 | GEO

Tau accumulation triggers STAT1-dependent memory deficits by suppressing NMDA receptor expression.

Project description:Intracellular tau accumulation forming neurofibrillary tangles is hallmark pathology of Alzheimer's disease (AD), but how tau accumulation induces synapse impairment is elusive. By overexpressing human full-length wild-type tau (termed hTau) to mimic tau abnormality as seen in the brain of sporadic AD patients, we find that hTau accumulation activates JAK2 to phosphorylate STAT1 (signal transducer and activator of transcription 1) at Tyr701 leading to STAT1 dimerization, nuclear translocation, and its activation. STAT1 activation suppresses expression of N-methyl-D-aspartate receptors (NMDARs) through direct binding to the specific GAS element of GluN1, GluN2A, and GluN2B promoters, while knockdown of STAT1 by AAV-Cre in STAT1flox/flox mice or expressing dominant negative Y701F-STAT1 efficiently rescues hTau-induced suppression of NMDAR expression with amelioration of synaptic functions and memory performance. These findings indicate that hTau accumulation impairs synaptic plasticity through JAK2/STAT1-induced suppression of NMDAR expression, revealing a novel mechanism for hTau-associated synapse and memory deficits.

| S-EPMC6549025 | biostudies-literature

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