Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Homo sapiens

SUBMITTER: Owen Robert Dando

PROVIDER: E-MTAB-14323 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

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

RNA-seq of triple cultures of neurons, astrocytes and microglia treated with blood clot conditioned media, lipopolysaccharide, and Nrf2-activating drug CDDO-TFEA.

Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). We found that myelomononuclear Nrf2 is active and protective after ICH in mice. To investigate the roles of myelomononuclear Nrf2 in modulating cell autonomous and non-cell autonomous responses to the oxidative and inflammatory consequences of ICH we developed an in vitro system of co-cultures of primary mouse microglia, human astrocytes and rat neurons and performed RNA-seq, subsequently performing in-silico separation of read data into separate species, and thus separate cell types. Cultures were treated with blood clot condition media (CCM), lipopolysaccharide (LPS), and Nrf2-activating drug CDDO-TFEA, and experiments were performed using wild-type mouse microglia, and microglia from mice with global Nrf2 deletion.

2024-08-13 | E-MTAB-14327 | biostudies-arrayexpress

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

Leukocyte dynamics after intracerebral hemorrhage in a living patient reveal rapid adaptations to tissue milieu

Project description:Intracerebral hemorrhage (ICH) is a devastating form of stroke with a high mortality rate and few treatment options. Discovery of therapeutic interventions has been slow given the challenges associated with studying acute injury, particularly over time, in the human brain. Inflammation induced by exposure of brain tissue to blood appears to be a major part of brain tissue injury. Here we longitudinally profiled blood and cerebral hematoma effluent from a patient enrolled in the Minimally Invasive Surgery with Thrombolysis in Intracerebral Haemorrhage Evacuation (MISTIEIII) trial, offering a rare window into the local and systemic immune responses to acute brain injury. Using single-cell RNA-sequencing, we characterized the local cellular response during ICH in the brain of a living patient at single-cell resolution for the first time. Our analysis revealed rapid shifts in the activation states of myeloid and T cells in the brain over time, suggesting that leukocyte responses are dynamically reshaped by the hematoma microenvironment. Interestingly, the patient had an asymptomatic re-bleed (second local exposure to blood) that our transcriptional data indicated occurred more than 30 hours prior to detection by CT scan. This case highlights the rapid immune dynamics in the brain after ICH and suggests that sensitive methods like scRNA-seq can inform our understanding of complex intracerebral events.

2021-06-02 | GSE166638 | GEO

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

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.

2022-04-29 | GSE200575 | 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

2013-01-19 | GSE43618 | GEO

Effect of Pterostilbene (PTE) treatment on gene expression after intracerebral hemorrhage injury

Project description:To investigate the effect of Pterostilbene(PTE) on gene expression after intracerebral hemorrhage injury, we employed RNA sequencing (RNA-seq) to profile the mRNA expression ensuing PTE treatment after ICH. Different gene distribution could be clearly seen on the volcano plot between diferent comparisions among Sham, ICH, and ICH+PTE group. Finally, we showed that 1021 shared genes overlapping between those differentially expressed genes, which was reversed by PTE treatment

2024-03-01 | GSE228222 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data