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RNA-seq analysis of tetrahedral nucleic acid nanomaterials loaded with miR-124 for the treatment of mouse intracerebral hemorrhage

ABSTRACT: We used collagenase injection into the brain to model intracerebral hemorrhage in mice. Simply put, the mice were immobilized on a stereotaxic frame. 0.05U collagenase VII was injected sequentially into the caudate nucleus (bregma: 0.2 mm anterior, 2.3 mm right lateral, and 3.5 mm deep). Three days after the collagenase injection, we collected brain tissue from normal mice (control group), the hemorrhagic side of the brain from ICH mice (experimental group), and the hemorrhagic side of the brain from ICH mice after intravenous injection of 20 mmol miR124-TNA (intervention group).

ORGANISM(S): Mus musculus

PROVIDER: GSE290311 | GEO | 2025/02/28

REPOSITORIES: GEO

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RNA-seq of microglia and monocyte-derived cells in Nrf2 knockout and wild-type mice after induced intracerebral hemorrhage or sham treatment

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor Nrf2, particularly in mononuclear myeloid cells (for example, monocyte-derived cells (MdC) and microglia), we sought to determine the importance of Nrf2 to mononuclear myeloid cell responses and their impact on ICH pathology. We used intrastriatal injection of collagenase to induce ICH in both wild-type mice, and knockout mice with Cx3cr1-Cre-mediated excision of Nrf2 (Nfe2l2) exon 5.

2024-08-13 | E-MTAB-14324 | biostudies-arrayexpress

Augmenting hematoma-scavenging capacity of innate immune cells by CDNF reduces brain injury and promotes functional recovery after intracerebral hemorrhage

Project description:We show that intracerebroventricular administration of recombinant human cerebral dopamine neurotrophic factor (rhCDNF) accelerates hemorrhagic lesion resolution, reduces peri-focal edema, and improves neurological outcomes in an animal model of collagenase-induced ICH. We demonstrate that CDNF acts on microglia/macrophages in the hemorrhagic striatum by promoting scavenger receptor expression, enhancing erythrophagocytosis and increasing anti-inflammatory mediators while suppressing the production of pro-inflammatory cytokines. Administration of rhCDNF results in upregulation of the Nrf2-HO-1 pathway, but alleviation of oxidative stress and unfolded protein responses in the perihematomal area. Finally, we demonstrate that intravenous delivery of rhCDNF has beneficial effects in an animal model of ICH and that systemic application promotes scavenging by the brain’s myeloid cells for the treatment of ICH.

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Analysis of Age-Dependent Transcriptomic Changes in Response to Intracerebral Hemorrhage in Mice

Project description:To investigate age-dependent transcriptomic changes between young or aged intracerebral hemorrhage mice, we established collagenase IV-induced intracerebral hemorrhage mice models. Intracerebral hemorrhage was induced by infusion of sterile collagenase IV in ipsilateral caudate putamen of brain. We then performed gene expression profiling analysis using data obtained from RNA-seq of brain perihematomal tissues from young or aged ICH mice 24 hours after intracerebral hemorrhage.

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Examining Transcriptomic Alterations in Rat Models of Intracerebral Hemorrhage and Severe Intracerebral Hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a life-threatening condition associated with significant morbidity and mortality. Understanding the molecular mechanisms underlying ICH and its severe form is crucial for developing effective therapeutic strategies. This study investigates transcriptomic alterations in rodent models of ICH and severe intracerebral hemorrhage to shed light on the genetic pathways involved in hemorrhagic brain injury. We performed principal component analysis, revealing distinct principal component segments of normal rats compared to intracerebral hemorrhage and severe intracerebral hemorrhage rats. We further employed heatmaps and volcano plots to identify differentially expressed genes and utilized bar plots and KEGG pathway analysis to elucidate the different molecular pathways involved. Using comprehensive RNA sequencing and bioinformatics analyses, we identified a multitude of differentially expressed genes in both the ICH and severe ICH models. Our results revealed 5679 common genes among the normal, intracerebral hemorrhage, and severe intracerebral hemorrhage groups in the upregulated genes group, and 1196 common genes in the downregulated genes. A volcano plot comparing the groups further highlighted common genes, including PDPN, TIMP1, SERPINE1, TUBB6, and CD44. These findings underscore the complex interplay of genes involved in inflammation, oxidative stress, and neuronal damage. Furthermore, pathway enrichment analysis uncovered key signaling pathways, including the TNF signaling pathway, protein processing in the endoplasmic reticulum, MAPK signaling pathway, and Fc gamma R-mediated phagocytosis, implicated in the pathogenesis of ICH.

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Regulation of Microglia-Mediated Neuroinflammation Post-Intracerebral Hemorrhage by Gut Microbiota and Short-Chain Fatty Acid Metabolism

Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).

2024-05-13 | GSE266602 | GEO

High-Throughput mRNA Sequencing Reveals Potential Therapeutic Targets of Febuxostat in Secondary Injury After Intracerebral Hemorrhage

Project description:Febuxostat is a urate-lowering medication for the treatment of patients with gout. This study was performed to elucidate the effects and underlying mechanisms of febuxostat on neuronal injury induced by intracerebral hemorrhage (ICH) in mice. The results showed that the administration of febuxostat improved neurological severity scores and blood-brain barrier (BBB) permeability. Moreover, febuxostat attenuated neuronal cell death and cytokine levels compared with the ICH group. Next, we conducted a transcriptome analysis of the neuroprotective effects of febuxostat. The overlapping significant differentially expressed genes (DEGs) were identified. Gene ontology (GO) analysis revealed that the overlapping significant DEGs were most enriched in five items. The intersecting DEGs of the aforementioned five pathways were Wisp1, Wnt7b, Frzb, and Pitx2. In addition, GO terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways revealed that DEGs were mainly involved in the wnt signaling pathway. Furthermore, the expression of Wisp1 and Wnt7b in the perihematomal region at 72 h post-ICH was observed. The results showed that both Wisp1 and Wnt7b were increased in the ICH group and were decreased by the administration of febuxostat. Taken together, the study showed that febuxostat protected against secondary brain injury after ICH and the Wnt7b-Wisp1 pathway was closely related to neuroprotective effects.

2022-06-09 | GSE193076 | GEO

Thioredoxin1 binding metastasis-associated lung adenocarcinoma transcript 1 attenuates inflammation and apoptosis after intracerebral hemorrhage

Project description:Post-transcriptional regulation and RNA-binding proteins (RBPs) play vital roles in the occurrence and secondary injury after intracerebral hemorrhage (ICH) and post-transcriptional regulation, respectively. Therefore, we screened out the differentially expressed RBPs after ICH and found thioredoxin1 (Txn1) as one of the most significantly differentially expressed RBPs. We also used an ICH model and in vitro experiments to investigate the role of Txn1 in clarifying the mechanism of Txn1 in ICH. First, we found that Txn1 was majorly expressed in microglia and neurons in the central nervous system, and its protein level was significantly reduced in perihematoma tissues. Furthermore, we established a Txn1-overexpressing ICH model by stereotaxic injection of adeno-associated virus (AAV) and discovered that the overexpression of Txn1 reduced secondary injury and improved prognosis after ICH. Moreover, to understand the mechanism of Txn1 after ICH, RNA immunoprecipitation combined with high-throughput sequencing (RIP-seq) showed that Txn1 binds to inflammation-and apoptosis-related mRNAs and affects RNA expression through RNA splicing and translational initiation. Finally, RNA pull-down assays and in vitro experiments confirmed that Txn1 binds to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) to reduce inflammation and apoptosis. Collectively, our results show that Txn1 reduces ICH-induced brain injury by affecting the post-transcriptional regulation of MALAT1. Consequently, Txn1 may represent a potential therapeutic target for alleviating ICH-induced brain injury.

2023-05-10 | GSE212595 | GEO

Next generation sequence of RNA in hematoma basal ganglia tissue of ICH mice model

Project description:To study the regulation of neuroinflammatory genes following an ICH insult, we induced ICH in C57 mice and analyzed the mRNA expression profile in the brain by RNA seq

2022-06-30 | GSE206971 | GEO

The critical role of MLKL in hemorrhagic stroke and the therapeutic potential of its associated protein network

Project description:MLKL, as the executor of necroptosis and a critical factor in the inflammation, has been shown to be associated with the progression of hemorrhagic stroke. Studies identified MLKL is a promoting factor in this process, suggesting its potential as a therapeutic target to mitigate post-hemorrhagic stroke damage. However, there is no direct evidence supporting MLKL as a drug target for hemorrhagic stroke currently, and the precise mechanisms by which MLKL functions in this context remain unclear. Here, we established an intracerebral hemorrhage model by collagenase IV injection and found that MLKL knockout alone was insufficient to fully reverse neuroinflammation and pathological damage. To further elucidate the molecular mechanisms underlying the effects of MLKL knockout on the ICH model, we conducted a proteomic analysis via LC-MS/MS. While MLKL knockout did not significantly reverse the damage caused by intracerebral hemorrhage, enhanced pathways related to inflammation, metabolism, and coagulation as well as attenuated functions related to neuron assemble were identified, suggesting that MLKL may exert its effects through these pathways. Based on these findings, we hypothesize that co-targeting MLKL and its associated protein network may yield better therapeutic outcomes for hemorrhagic stroke.

2024-09-27 | PXD056595 |

Expression data from human brain samples

Project description:Spontaneous intracerebral hemorrhage (ICH) represents about 15% of all strokes and is associated with high mortality rates. Our aim was to identify the gene expression changes and biological pathways altered in the brain following ICH. Twelve brain samples were obtained from four deceased patients who suffered an ICH including perihematomal tissue (PH) and the corresponding contralateral white (CW) and grey (CG) matter. Brain samples from 4 deceased patients who had a supratentorial intracerebral hemorrhage within the previous 4 days were included in the microarray study. This study group included 2 women and 2 men with a median age of 79 (68-92). On autopsy and during macroscopic exam, perihematomal areas suspected to present edema were identified by an experienced neuropathologist using last available neuroradiology images. Samples from perihematomal areas (PH), contralateral grey matter (CG) and contralateral white matter (CW) were obtained within the first 5 h after death and snap frozen in liquid nitrogen and stored at -80ºC until RNA isolation.

2010-09-23 | E-GEOD-24265 | biostudies-arrayexpress

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