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Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [RNA-Seq]

ABSTRACT: Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [RNA-Seq]

PROVIDER: PRJNA1226545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32452076_1.fastq.gz	Fastqsanger.gz
	SRR32452076_2.fastq.gz	Fastqsanger.gz
	SRR32452077_1.fastq.gz	Fastqsanger.gz
	SRR32452077_2.fastq.gz	Fastqsanger.gz
	SRR32452078_1.fastq.gz	Fastqsanger.gz

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Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [RNA-Seq]

Project description:Ischemic stroke recovery involves dynamic interactions between the central nervous system and infiltrating immune cells. Peripheral immune cells compete with resident microglia for spatial niches in the brain, but how modulating this balance affects recovery remains unclear. Here, we use PLX5622 to create spatial niches for peripheral immune cells, altering the competition between infiltrating immune cells and resident microglia in male mice following transient middle cerebral artery occlusion (tMCAO). We find that early-phase microglia attenuation promotes long-term functional recovery. This intervention amplifies a subset of monocyte-derived macrophages (RAMf) with reparative properties, characterized by high expression of GPNMB and CD63, enhanced lipid metabolism, and pro-angiogenic activity. Transplantation of RAMf into stroke-affected mice improves white matter integrity and vascular repair. We identify Mafb as the transcription factor regulating the reparative phenotype of RAMf. These findings highlight strategies to optimize immune cell dynamics for post-stroke rehabilitation.

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Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [scRNA-Seq]

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Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [scRNA-Seq]

Project description:Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery [scRNA-Seq]

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Glycogen stress granules cause astrocytic mitochondrial dysfunction to aggravate ischemic damage and delay recovery after stroke

Project description:Ischemic stroke induces pathological glycogen deposition in astrocytes, but its role in post-injury neural dysfunction remains undefined. We reveal that glycogen-laden astrocytes in the ischemic penumbra undergo HDAC3-dependent mitochondrial fragmentation via a stress granule-mediated mechanism, exacerbating neuronal injury and hindering functional recovery. Mechanistic studies demonstrate that glycogen aggregates sequester cytoplasmic HDAC3, enabling its translocation to mitochondria. There, HDAC3 deacetylates outer mitochondrial membrane protein ATAD3A, promoting oligomerization-driven mitochondrial fission. Astrocyte-specific ATAD3A ablation prevents stroke-induced synaptic disorganization, neural circuit disruption, and cognitive deficits. Therapeutically, combined administration of cotadutide (a glycogen-depleting GLP-1/GCGR agonist) and HDAC3 inhibitor RGFP966 reverses glycogen accumulation, rescues mitochondrial architecture/function, and restores synaptic plasticity and circuit reorganization, thereby accelerating sensorimotor recovery. Our work identifies glycogen stress granules as pathogenic signaling hubs linking astrocytic metabolic stress to mitochondrial failure through compartmentalized HDAC3-ATAD3A crosstalk, and proposes a dual-target paradigm addressing both substrate overload and protein acetylation dynamics for stroke neurorestoration.

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microRNAs involved in regulating embolic stroke recovery following spontaneous reperfusion [miRNA]

Project description:To date, miRNA expression studies on cerebral ischemia in both human and animal models have focused mainly on acute phase of ischemic stroke. In this study, we present the roles played by microRNAs in the spontaneous recovery phases in cerebral ischemia using rodent stroke models. In this study presented here, Middle Cerebral Artery Occlusion stroke model was established by using embolus and the brain samples of stroke model were harvested at 0hrs, 3hrs, 6hrs, 12hrs, 24hrs, 48hrs, 72hrs, 120hrs and 168hrs. RNAs were extracted from these samples and microRNA array and mRNA array were performed.

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microRNAs involved in regulating embolic stroke recovery following spontaneous reperfusion [mRNA]

Project description:To date, miRNA and mRNA expression studies on cerebral ischemia in both human and animal models have focused mainly on acute phase of ischemic stroke. In this study, we present the roles played by microRNAs in the spontaneous recovery phases in cerebral ischemia using rodent stroke models. In this study presented here, Middle Cerebral Artery Occlusion stroke model was established by using embolus and the brain samples of stroke model were harvestd at 0hrs, 3hrs, 6hrs, 12hrs, 24hrs, 48hrs, 72hrs, 120hrs and 168hrs. RNAs were extracted from these samples and microRNA array and mRNA array were performed.

2013-12-09 | E-GEOD-46267 | biostudies-arrayexpress

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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microRNAs involved in regulating embolic stroke recovery following spontaneous reperfusion [miRNA]

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Expression data from heart tissue after induction of ischemic stroke (occlusion of the middle cerebral artery)

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