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Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke

ABSTRACT: Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke

PROVIDER: PRJNA908099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22516039_1.fastq.gz	Fastqsanger.gz
	SRR22516039_2.fastq.gz	Fastqsanger.gz
	SRR22516040_1.fastq.gz	Fastqsanger.gz
	SRR22516040_2.fastq.gz	Fastqsanger.gz
	SRR22516041_1.fastq.gz	Fastqsanger.gz

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Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [RNA-seq]

Project description:The rapid accumulation of self-renewed polarized microglia in the penumbra is the critical neuroinflammatory process after the onset of ischemic stroke, leading to secondary demyelination and neuronal loss. HDAC3 has been reported to regulate cell proliferation of tumour cells and modulate neuroinflammation. However, the mechanism by which HDAC3 regulates microgliosis and microglial polarization remains ambiguous. Herein, we demonstrated that microglia-specific ablation of HDAC3 (HDAC3-miKO) ameliorated poststroke long-term functional and histological outcomes. Starting with unbiased RNA seq of microglia, we identified mitosis as the most significant process reversed by loss of HDAC3. Notably, HDAC3-miKO specifically inhibited the proliferation of M1-like microglia but not M2-like microglia, resulting in microglial transition to an M1-like state. Moreover, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) revealed that HDAC3 deletion induced drastic closing of accessible regions enriched with motifs for PU.1. Taken together, we uncovered for the first time that HDAC3/PU.1-mediated differential proliferation-related reprogramming in different microglia populations drives poststroke inflammatory state transition of microglia and thereby contributes to the pathophysiology of ischemic stroke.

2024-03-13 | GSE220042 | GEO

Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [ATAC-seq]

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Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [ATAC-seq]

Project description:Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [ATAC-seq]

| PRJNA908102 | ENA

Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [RNA-seq]

Project description:Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke [RNA-seq]

| PRJNA908103 | ENA

Arresting the bad seed: HDAC3 regulates proliferation of different microglia after ischemic stroke

Project description: Not available

| S-EPMC10917353 | biostudies-literature

Arresting the Bad Seed: HDAC3 Regulates Proliferation of Different Microglia after Ischemic Stroke

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

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Exome sequencing of stroke cases with good or bad recovery three months after stroke

Project description:With the aim to identify rare genetic variation involved in stroke recovery, this is a pilot study on extreme phenotypes of good and bad recovery. Exome sequencing was performed on 41 and 49 samples in the bad and good recovery subset, respectively. Rare Variant association Analysis was performed on the exome sequencing results.

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Gene expression analysis of peripheral whole blood RNA following ischemic stroke

Project description:The purpose of this project was to elucidate gene expression in the peripheral whole blood of acute ischemic stroke patients to identify a panel of genes for the diagnosis of acute ischemic stroke. Peripheral blood samples were collected in Paxgene Blood RNA tubes from stroke patients who were >18 years of age with MRI diagnosed ischemic stroke and controls who were non-stroke neurologically healthy. The results suggest a panel of genes can be used to diagnose ischemic stroke, and provide information about the biological pathways involved in the response to acute ischemic stroke in humans. Total RNA extracted from whole blood in n=39 ischemic stroke patients compared to n=24 healthy control subjects.

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Project description:We performed a genome-wide methylation study in whole-blood DNA from 404 ischemic stroke patient cohort, distributed across 3 ischemic stroke subtypes: Large-artery atherosclerosis (n=132), Small-artery disease (n=141) and Cardio embolic (n=127) . Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites. We performed a genome-wide methylation study in whole-blood DNA from 185 ischemic stroke patient cohort. Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites.

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Project description:Analysis of astrocytic gene expression profiles after ischemic stroke. Stroke is a complicated disease caused by the interaction of multiple celltypes. Results provide new insights into the molecular mechanisms underlying astrocytic activation after ischemic stroke.

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