Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260047 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression of cell cycle related-genes after early cerebral ischemia in a mouse thrombotic stroke model: a transcriptomic coexpression analysis.
2017-08-27 | GSE60820 | GEO
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.
2013-12-09 | E-GEOD-46266 | biostudies-arrayexpress
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
Project description:Brain ischemia causes disruption in cerebral blood flow and blood–brain barrier integrity, which are normally maintained by astrocyte endfeet. Emerging evidence points to dysregulation of the astrocyte translatome during ischemia, but its effects on the endfoot translatome are unknown. In this study, we aimed to investigate the early effects of ischemia on the astrocyte endfoot translatome in a rodent cerebral ischemia and reperfusion model of stroke. To do so, we immunoprecipitated astrocyte-specific tagged ribosomes (RiboTag IP) from mechanically isolated brain microvessels. In mice subjected to middle cerebral artery occlusion and reperfusion and contralateral controls, we sequenced ribosome-bound RNAs from perivascular astrocyte endfeet and identified 205 genes that were differentially expressed in the endfoot translatome after ischemia. The main biological processes associated with these differentially expressed genes included proteostasis, inflammation, cell cycle/death, and metabolism. Transcription factors whose targets were enriched amongst upregulated translating genes included HSF1, the master regulator of the heat shock response. The most highly upregulated genes in the translatome were HSF1-dependent Hspa1a and Hspa1b, which encode the inducible HSP70. Using qPCR, Western blot, and immunohistochemistry, we confirmed that HSP70 is upregulated in astrocyte endfeet after ischemia. This coincided with an increase in ubiquitination across the proteome that suggests that ischemia induces a disruption in proteostasis in astrocyte endfeet. These findings suggest a robust proteostasis response to proteotoxic stress in the endfoot translatome after ischemia. Modulating proteostasis in endfeet may be a strategy to preserve endfoot function and BBB integrity after ischemic stroke.
2025-01-27 | GSE286075 | GEO
Project description:Immune responses and neuroinflammation occurring after acute ischemic stroke (AIS) are closely related to brain injury. Histone lactylation is a metabolic stress-related histone modification that participates in the pathogenesis of various diseases. However, the role of histone regulation in cerebral ischemic stroke remains unknown. In this study, a transient middle cerebral artery occlusion (tMCAO/R) model and an oxygen–glucose deprivation and reoxygenation (OGD/R) model were used to simulate in vivo/in vitro ischemia–reperfusion injury. The underlying mechanism of microglial histone lactylation was investigated using microglia-specific SMEK1-overexpressing mice and BV2 cells. The results showed that lactate overload resulted in elevated histone lactylation after AIS. Decreased SMEK1 expression in microglia after ischemic stroke was associated with increased lactate levels and subsequent neuroinflammation. Microglia-specific SMEK1 deficiency in microglia after ischemia can promote lactate production by inhibiting the pyruvate dehydrogenase kinase 3-pyruvate dehydrogenase (PDK3-PDH) pathway. Specifically, H3 lysine 9 lactylation (H3K9la) activated Ldha and Hif-1α transcription in microglia and promoted glycolysis. SMEK1-overexpressing mice exhibited better neurologic recovery after ischemic stroke than control mice. Mechanistically, we provided new evidence that microglial histone lactylation promoted glycolysis in ischemia‒reperfusion injury and elucidated the potential role of SMEK1 as an upstream regulatory molecule in histone lactylation after cerebral ischemia. According to our results, microglial SMEK1 may be potential therapeutic targets for AIS.
2025-01-02 | GSE283233 | GEO
Project description:The goals of this study are to compare hippocampus transcriptome profiling (RNA-seq) after Cerebral Ischemia 1.5 h Reperfusion 24 h in mouse stroke model
2024-02-10 | GSE202391 | GEO
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.
2013-12-09 | GSE46266 | GEO
Project description:Stroke remains a major leading cause of death and disability worldwide. Despite continuous advances, the identification of key molecular signatures of ischemic stroke within the hyper-acute phase of the disease is still of primary interest for a real translational research on stroke diagnosis, prognosis and treatment. High-throughput - omics technologies are enabling large-scale studies on stroke pathology at different molecular levels. Data integration resulting from these -omics approaches is becoming crucial to unravel the interactions among all different molecular elements and highly contribute to interpret all findings in a complex biological context. Here, we have used advanced data integration methods for multi-level joint analysis of transcriptomics and proteomics datasets depicted from the mouse brain 2h after cerebral ischemia. By modeling network-like correlation structures, we identified a set of differentially expressed genes and proteins by ischemia with a relevant association in stroke pathology. The ischemia-induced deregulation of 10 of these inter-correlated elements was successfully verified in a new cohort of ischemic mice, and changes in their expression pattern were also evaluated at a later time-point after cerebral ischemia. Of those, CLDN20, GADD45G, RGS2, BAG5 and CTNND2 were highlighted and evaluated as potential blood biomarkers of cerebral ischemia in blood samples from ischemic and sham-control mice and from ischemic strokes and other patients presenting stroke-mimicking conditions. Our findings indicated that CTNND2 and GADD45G levels in blood within the first hours after ischemic stroke might be potentially useful to discriminate ischemic strokes from mimics and to predict patients’ poor outcome after stroke, respectively. In summary, we have here used for the first time an integrative approach to elucidate by means of biostatistical tools key elements of the initial stages of the stroke pathophysiology, highlighting new outstanding proteins that might be further considered as blood biomarkers of ischemic stroke.
2020-09-02 | PXD016538 | Pride
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.
2013-12-09 | GSE46267 | GEO
Project description:Sleep deprivation (SD) performed before stroke induces an ischemic tolerance state as observed in other forms of preconditioning. As the mechanisms underlying this effect are not well understood we used DNA oligonucleotide microarray analysis, to identify the genes and the gene-pathways underlying SD preconditioning. Gene expression was analyzed 3 days after stroke surgery in four experimental groups: i) SD performed before focal cerebral ischemia induction; ii) SD performed before Sham surgery; iii) IS without SD; and iv) Sham surgery without SD. SD was performed by gentle handling during the last 6h of the light period and ischemia was induced immediately after. Stroke induced a massive alteration in gene expression both in sleep deprived and non-sleep deprived animals. However, compared to animals that underwent ischemia alone, SD induced a general reduction in transcriptional changes with a reduction in the upregulation of genes involved in cell cycle regulation and immune response. Moreover an upregulation of a new neuroendocrine pathway which included melanin concentrating hormone, glycoprotein hormones-M-kM-1-polypeptide and hypocretin was observed exclusively in rats sleep deprived before stroke. Our data indicate that SD before stroke reprogrammed the signaling response to injury. The inhibition of cell cycle regulation and inflammation are neuroprotective mechanisms reported also for other forms of preconditioning treatment whereas the implication of the neuroendocrine function is novel and has never been described before. These results therefore provide new insights into neuroprotective mechanisms involved in ischemic tolerance mechanisms.
2015-10-30 | E-MTAB-3148 | biostudies-arrayexpress