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Sustaining microglial reparative function enhances stroke recovery [ATAC-seq]

ABSTRACT: To investigate time-dependent changes in the epigenetic chromatin state in microglia after ischemic stroke, we performed assay for transposase-accessible chromatin with sequencing (ATAC-seq) of microglia from mouse brains at multiple time points after middle cerebral artery occlusion (MCAO).

ORGANISM(S): Mus musculus

PROVIDER: GSE319235 | GEO | 2026/03/11

REPOSITORIES: GEO

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Sustaining microglial reparative function enhances stroke recovery [Bulk RNA-seq]

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Sustaining microglial reparative function enhances stroke recovery [scRNA-seq]

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Sustaining microglial reparative function enhances stroke recovery [HiChIP]

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Sustaining microglial reparative function enhances stroke recovery [CUT&Tag]

Project description:To investigate YY1 and ZFP384 binding in microglia and the microglial cell line after ischemic stroke, we performed cleavage under targets and tagmentation (CUT&Tag) analysis using anti-YY1 and anti-ZFP384 antibodies.

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TGFβ-activated kinase 1-dependent microglial and macrophage responses aggravate long-term outcomes after ischemic stroke

Project description:Microglia/macrophages (Mi/MΦ) can profoundly influence stroke outcomes by acquiring functionally dominant phenotypes (pro-inflammatory or anti-inflammatory; neurotoxic or neuroprotective). Identification of the molecular mechanisms that dictate the functional status of Mi/MΦ after brain ischemia/reperfusion may reveal novel therapeutic targets for stroke. We hypothesized that activation of TGFβ-activated kinase 1 (TAK1), a key MAP3K upstream of multiple inflammation-regulating pathways, drives Mi/MΦ towards a pro-inflammatory phenotype and potentiates ischemia/reperfusion brain injury. Young adult mice were subjected to 1 h of middle cerebral artery occlusion (MCAO) followed by reperfusion. TAK1 was targeted by tamoxifen-induced Mi/MΦ-specific knockout (mKO). Mi/MΦ functional status and brain inflammatory profiles were assessed 3 days after MCAO by RNA-seq of flow cytometry-sorted brain Mi/MΦ. The results showed that TAK1 promotes ischemia/reperfusion-induced inflammation, brain injury, and maladaptive behavior by enhancing pro-inflammatory and neurotoxic Mi/MΦ responses.

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Repair-Associated Macrophages Increase after Early-phase Microglia Attenuation to Promote Ischemic Stroke Recovery

Project description:<p>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.</p>

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High-Frequency Repetitive Transcranial Magnetic Stimulation (rTMS) Protects Against Ischemic Stroke by Inhibiting M1 Microglia Polarization through Let-7b-5p/HMGA2/NF-κB Signaling Pathway

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Project description:Post-stroke depression (PSD) is a common but severe mental complication after stroke. However, the cellular and molecular understanding of PSD is still yet to be illustrated. In current study, we prepared PSD rat model (MD) via unilateral middle cerebral artery occlusion (MCAO) and chronic stress stimulation (DEPR), and isolated hippocampal tissues for single cell sequencing of 10x Genomics Chromium. This study characterized the single cell expression profile of hippocampal PSD, and unmask the differential expressed genes of endothelium, microglia and oligodendrocytes, emphasizing the crosstalk among them to provide theoretical basis for the in-depth mechanism research and drug therapy of PSD.

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TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2

Project description:Stroke is a kind of cerebrovascular disease with high mortality. TMAO has been shown to aggravate stroke outcomes, but its mechanism remains unclear. Mice were treated with TMAO in normal saline by oral gavage for 14 consecutive days. Then, mice were made into MCAO models. Neurological score, infarct volume, neuronal damage and markers associated with inflammation were assessed. Since microglia played a crucial role in stroke, microglia of MCAO mice were isolated for high-throughput sequencing to identify the most differentially expressed gene following TMAO treatment. Afterward, the downstream pathways of TMAO were investigated using primary microglia. Our results demonstrated that TMAO promoted the release of inflammatory cytokines in the brain of MCAO mice and promoted the activation of OGD/R microglial inflammasome, thereby exacerbating stroke outcomes. FTO/IGF2BP2 inhibited NLRP3 inflammasome activation in OGD/R microglia by downregulating the m6A level of NLRP3, TMAO can inhibit the expression of FTO and IGF2BP2, thus promoting the activation of NLRP3 inflammasome in OGD/R microglia. In conclusion, these results demonstrated that TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2.

2023-09-06 | GSE216349 | GEO

Retinoid X Receptor as a Mediator of Post Stroke Recovery by Reversing Age-Associated Phenotypes of Microglia/Hematogenous Macrophages

Project description:After stroke, microglia/blood-derived macrophages, together MF, clear dead cells and cellular debris in the infarcted brain through phagocytosis as an essential part of the repair/recovery process. However, the phagocytic capability of MF declines with age. Furthermore, aged MF become overactivated in response to stroke, enhancing secondary brain injury. Now, demonstrate that by reversing the age-related dysfunctions in MF through activating the retinoid x receptor (RXR), the recovery after stroke in the aged brain could be improved. Using RNA sequencing, we compared the transcriptomes between MF isolated from the brains of young and aged mice. We observed higher levels of pro-inflammatory genes and lower levels of phagocytosis-facilitating genes (Cd206, Cd36) expressed by aged MF. Meanwhile, the treatment with RXR agonist bexarotene (BEX) reversed the signature genes of microglia aging in the aged MF. With the in vivo phagocytosis model, we showed that BEX enhanced the phagocytic ability of aged MF. Using mouse MCAo stroke model, we established that BEX improved sensorimotor and cognitive recovery after MCAo in a myeloid-RXRa-specific and -dependent manner. In conclusion, we showed that activating RXRa partially restores age-related MF dysfunctions and that RXRa deficiency in MF limits the therapeutic effect of RXR in improving post-stroke recovery in the aged brain

2025-09-17 | GSE287142 | GEO

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