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Loss of TSPOAP1 exacerbates mitochondrial dysfunction and neuronal apoptosis after intracerebral hemorrhage

ABSTRACT: Intracerebral hemorrhage (ICH) induces severe secondary neuronal injury, in which mitochondrial dysfunction and apoptosis play central roles. Accumulating evidence suggests that mitochondrial failure represents a critical convergence point linking diverse injurious stimuli to neuronal apoptosis after ICH. However, the molecular mechanisms that connect mitochondrial dysfunction to irreversible apoptotic commitment remain incompletely understood. In particular, the upstream regulators governing mitochondrial permeability transition pore (mPTP) opening during ICH have yet to be fully defined.

ORGANISM(S): Homo sapiens

PROVIDER: GSE338415 | GEO | 2026/07/13

REPOSITORIES: GEO

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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.

2024-06-11 | GSE264394 | GEO

Transcriptomic profiling identifies Forl1 as a potential therapeutic target in intracerebral hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a severe subtype of stroke characterized by high mortality and disability, while effective therapeutic targets remain limited. To identify key regulatory molecules involved in ICH pathogenesis, we established a mouse model of intracerebral hemorrhage and performed RNA sequencing (RNA-seq) analysis on peri-hematomal brain tissues. Three ICH mice and three sham-operated mice were included in this study. Differential expression analysis revealed a series of significantly dysregulated genes following ICH, among which Forl1 was markedly downregulated. Functional enrichment analysis suggested that these altered genes were associated with inflammatory response, immune regulation, neuronal injury, and tissue repair pathways. The present dataset provides transcriptomic evidence supporting the potential role of Forl1 in ICH progression and may contribute to the identification of novel therapeutic targets for intracerebral hemorrhage.

2026-05-16 | GSE330577 | GEO

RNA-seq of perihaematomal and anatomically matched contralateral brain tissue after intracerebral hemorrhage

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, we performed bulk RNA sequencing of perihaematomal and anatomically matched contralateral brain homogenate obtained at autopsy from a cohort of patients who died either within 24h of ICH or between 4-14 days of ICH onset, to investigate the spatiotemporal evolution of this Nrf2 activation.

2024-08-13 | E-MTAB-14323 | biostudies-arrayexpress

Loss of TSPOAP1 exacerbates mitochondrial dysfunction and neuronal apoptosis after intracerebral hemorrhage

Project description:Loss of TSPOAP1 exacerbates mitochondrial dysfunction and neuronal apoptosis after intracerebral hemorrhage

| PRJNA1494460 | ENA

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

Development of gene expression signatures in experimental intracerebral hemorrhage

Project description:To identify the potential lncRNA and mRNA post intracerebral hemorrhage (ICH), we have employed lncRNA microarray expression profiling. 570 mRNAs and 313 lncRNAs were identified in the ICH vs sham group .Expression of six mRNA (Saa3, Col10a1, Mmp13, Oxt, Pcdhb6 and Resp18) and lncRNA (ENSMUT00000141700, AK143011, ENSMUT00000128306, AK030988, ENSMUST00000187076 and ENSMUST00000134129) from this signature was quantified by qPCR.

2023-05-17 | GSE227683 | GEO

Identification of inflammation-related microRNAs deregulated in the plasma from intracerebral hemorrhage patients

Project description:We tested the hypothesis that circulating microRNAs (miRNAs) present in plasma might display a specific signature in patients with intracerebral hemorrhage (ICH). Global miRNA profiles were determined with the Agilent Human miRNA Microarray platform, 027233. ICH patients display a characteristic inflammation-related miRNA profile as compared to healthy controls. Plasma samples were collected from the following 6 subject groups: male ICH patients (n=8), female ICH patients (n=7), male healthy control (n=4), female healthy control (n=4), male ischemic stroke patients (n=8) and female ischemic stroke patients (n=8). Total RNAs isolated from 1 ml plasma were pooled for each group. A fixed volume of RNA sample was withdrawn from each pool and used for microarray detection.

2013-01-19 | E-GEOD-43618 | biostudies-arrayexpress

Genome-wide DNA methylation pattern in whole blood associated with primary intracerebral hemorrhage

Project description:To reveal the role of DNA methylation in peripheral blood from primary intracerebral hemorrhage(ICH) ,DNAs from 30 ICH patients and 34 matched controls were analyzed by methylation microarray. In total, we identified 1377 hypomethylated and 153 hypermethylated differentially methylated positions (DMPs) in peripheral blood from ICH patients compared to healthy controls.

2021-07-10 | GSE179759 | GEO

Targeted Deletion of EMMPRIN in Microglia/Macrophages Mitigates Neuronal Death in Intracerebral Hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a devastating subtype of stroke with high mortality and limited therapeutic options. Microglia and macrophages are myeloid cells that are rapidly recruited into ICH lesions where they contribute to secondary brain injury. However, the driver of myeloid cell neurotoxicity remains incompletely understood. Here, we interrogated extracellular matrix metalloproteinase inducer (EMMPRIN, CD147) in promoting microglia/macrophage neurotoxicity in ICH. Using both AAV-mediated knockdown and CX3CR1Cre:EMMPRINfl/fl mice, we demonstrate that EMMPRIN deletion in microglia/macrophages reduced neuronal death and improved functional recovery after ICH. EMMPRIN-mediated neurotoxicity in ICH was associated with elevation of matrix metalloproteinases, and reduced signaling through the p38/MAPK, MEF2C transcription factor and Bcl2 anti-apoptotic pathway. Correspondent with lower injury, EMMPRIN deletion enhanced neurogenesis and oligodendrogenesis in ICH. These findings establish EMMPRIN elevation in myeloid cells as a prominent regulator of ICH pathophysiology and a promising therapeutic target to limit secondary injury and promote brain repair.

2026-01-26 | PXD063205 | Pride

Gut microbiota dysbiosis and neurological function recovery after intracerebral hemorrhage [16S rRNA-Seq]

Project description:We aimed to investigate the microbial community composition in patients with intracerebral hemorrhage (ICH) and its effect on prognosis. The relationship between changes in bacterial flora and the prognosis of spontaneous cerebral hemorrhage was studied in two cohort studies. Fecal samples from healthy volunteers and patients with intracerebral hemorrhage were subjected to 16S rRNA sequencing at three time points: T1 (within 24 hours of admission), T2 (3 days post-surgery), and T3 (7 days post-surgery) using Illumina high-throughput sequencing technology.

2024-08-22 | E-MTAB-14351 | biostudies-arrayexpress

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