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Effects of NMDAR on mouse hippocampal neuron (HT22) mRNA and lncRNA expression during hypoxia/reoxygenation injury

ABSTRACT: To investigate the changes of the transcriptome in neuronal cells under the condition of NMDAR hypofunction and H/R injury, we compared the changes of mRNA and lncRNA expression levels in mouse hippocampal neuron HT22 cell with or without NMDAR knockdown and H/R stimulation by RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE214716 | GEO | 2022/10/10

REPOSITORIES: GEO

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Effects of NMDAR on mouse hippocampal neuron (HT22) proteome expression during hypoxia/reoxygenation injury

Project description:Brain tissue is extremely sensitive to hypoxia/reoxygenation (H/R) injury, which can easily cause irreversible damage to neurons. H/R injury could induce neuronal apoptosis through glutamate-mediated excitotoxicity. N-methyl-d-aspartate receptor (NMDAR) is one of the main receptors of excitatory glutamate, and blocking NMDAR could protect brain tissue from ischemia and hypoxia injury. NMDAR hypofunction can also cause psychotic symptoms or cognitive impairment. However, there is still a lack of systematic research on the changes of the proteome and transcriptome in neuronal cells under the condition of NMDAR hypofunction and H/R injury. In this study, we compared the changes of proteome expression levels in neurons after NMDAR knockdown and H/R stimulation by isobaric tags for relative and absolute quantitation (iTRAQ).

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Effects of NMDAR on mouse hippocampal neuron (HT22) mRNA and lncRNA expression during hypoxia/reoxygenation injury

Project description:Effects of NMDAR on mouse hippocampal neuron (HT22) mRNA and lncRNA expression during hypoxia/reoxygenation injury

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Chromatin Immunoprecipitation analysis of mouse hippocampal neuron HT22 cells

Project description:We used H4K5bu and H4K5ac antibodies to specifically enrich mouse hippocampal neuronal cells (HT22) before and after BHBA administration. We found that the acetylation and butylation of histone H4K5 play a key role in the neuroprotection of BHBA.

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Human NMDAR autoantibodies disrupt excitatory-inhibitory balance leading to hippocampal network hypersynchrony

Project description:Specific autoantibodies against the NMDA-receptor (NMDAR) GluN1 subunit cause severe and debilitating NMDAR-encephalitis. Autoantibodies induce prototypic disease symptoms resembling schizophrenia, including psychosis and cognitive dysfunction. Using a mouse passive transfer model applying human monoclonal anti-GluN1-autoantibodies, we observed CA1 pyramidal neuron hypoexcitability, reduced AMPA-receptor (AMPAR) signaling, and faster synaptic inhibition resulting in disrupted excitatory-inhibitory balance. Functional alterations were supported by widespread remodeling of the hippocampal proteome, including changes in glutamatergic and GABAergic neurotransmission. At the network level, anti-GluN1-autoantibodies amplified gamma oscillations and disrupted theta-gamma coupling. A data-informed network model revealed that lower AMPAR strength and faster GABAA-receptor current kinetics chiefly account for these abnormal oscillations. As predicted by our model and evidenced experimentally, positive allosteric modulation of AMPARs alleviated aberrant gamma activity and thus reinforced the causative effects of the excitatory-inhibitory imbalance. Collectively, NMDAR-hypofunction-induced aberrant synaptic, cellular, and network dynamics provide new mechanistic insights into disease symptoms in NMDAR-encephalitis and schizophrenia.

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChipM-BM-. Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour. The gene expression profile from the J147-treated HT22 cells (1 hour exposure) was compared to HT22 cells treated with vehicle only (DMSO) for 1 hour. The DMSO/vehicle treated cells serve as the control and are referred to as untreated with drug.

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Chromatin Immunoprecipitation analysis of mouse hippocampal neuron HT22 cells

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Chromatin profiling in HT22 hippocampal cells

Project description:Chromatin profiling in HT22 hippocampal cells

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.

2013-03-28 | GSE45534 | GEO

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