Gene expression profiles of endothelium, microglia and oligodendrocytes in hippocampus of post-stroke depression rat at single cell resolution
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE232936 | GEO | 2023/05/24
REPOSITORIES: GEO
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Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study. Total RNA isolated from sham, MCAo and MCAo+nPLA rat brains, was pooled to minimize inter-individual variation and hybridized to each array of the RAE-230A or U34A GeneChipTM according to protocols described in the GeneChipTM expression analysis package (Affymetrix, CA).
2009-09-04 | E-GEOD-17929 | biostudies-arrayexpress
Project description:Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study.
2009-09-04 | GSE17929 | GEO
Project description:Reactive astrogliosis is characterized by a profound change in astrocyte phenotype in response to all CNS injuries and diseases. To better understand the reactive astrocyte state, we used Affymetrix GeneChip arrays to profile gene expression in populations of reactive astrocytes isolated at various time points after induction using two different mouse injury models, ischemic stroke and neuroinflammation. Young adult male mice underwent middle cerebral artery occlusion (MCAO) to produce ischemic stroke or control sham surgery. Young adult mice were injected intraperitoneally with 5 mg/kg lipopolysaccharide (LPS) to produce neuroinflammation or saline for control. Astrocytes were acutely purified from control and injured brains at 1 day after injury for LPS/saline injection and 1, 3 days and 7 days after MCAO/sham surgeries.
2012-05-01 | E-GEOD-35338 | biostudies-arrayexpress
Project description:To investigate the potential involvement of circRNA in ischemic pathophysiology, we performed a circRNA microarray in an established transient middle cerebral artery occlusion (MCAO) mouse model of stroke. We evaluated the expression of 1797 circRNAs in adult mice brain after tMCAO. In our study, 5 of the 1178 circRNAs analyzed in the circRNA array were up-regulated significantly, ≥1.5-fold, in ischemic cortex at 12 hours of reperfusion after MCAO compared with their levels in sham group.
2020-09-25 | GSE115697 | GEO
Project description:Astrogliosis is a hallmark of the response to brain ischemia, comprised of changes in gene expression and morphology. Hsp72 protects from cerebral ischemia, and although several mechanisms of protection have been investigated, effects on astrocyte activation are unknown. To identify potential mechanisms of protection, gene expression was assessed in mice subjected to middle cerebral artery (MCAO) or sham surgery, of either wildtype (WT) or Hsp72-overexpressing (Hsp72Tg) mice. After stroke, both genotypes exhibited genes related to cell death, stress response, and immune response. Furthermore, genes indicative of astrocyte activation, including cytoskeletal proteins and cytokines, were upregulated. To measure astrocyte activation after stroke, detailed histological and morphological analyses were performed in the cortical penumbra after stroke using unbiased stereology. Consistent with other reports, we observed a marked and persistent increase in glial fibrillary acidic protein (GFAP ) as soon as 3 hours after MCAO. In contrast, vimentin immunoreactivity appeared 12-24 hours after stroke, peaked at 72 hours, and returned to baseline after 30 days. Surprisingly, no change in overall astrocyte number was observed based on glutamine synthetase (GS) immunoreactivity. To determine if Hsp72Tg mice exhibited altered astrocyte activation compared to WT controls, morphological evaluation by fractal analysis was used. Overexpression of Hsp72 reduced astrocyte cell area, arbor area, and to a lesser extent fractal dimension, 72 hours following stroke. In conclusion, in vivo overexpression of Hsp72 alters gene expression following stroke, including genes involved in astrocyte activation, and decreases astrocyte activation acutely following MCAO. Thus, modulation of astrogliosis may be a neuroprotective mechanism exerted by Hsp72 after ischemia. A total of 10 samples were analyzed, with 5 of each genotype, wildtype (WT) and Hsp72-overexpressing (Hsp72Tg) mice. Of the 5 in each group, 3 received middle cerebral artery occlusion (MCAO) and 2 received a sham surgery. The sham samples serve as the controls for the MCAO samples in each genotype. All samples were taken from the ischemic or control hemisphere 24 hours after surgery.
2013-01-11 | E-GEOD-28731 | biostudies-arrayexpress
Project description:<p><em>Gastrodia elata</em> Blume (GE) has been widely used to treat various central and peripheral nerve diseases, and P-Hydroxybenzaldehyde (PHBA) is one of the indicative components of GE brain protection. Since the previous study of our group found that PHBA has a good effect on protecting mitochondria against cerebral ischemia-reperfusion injury in rats (I/R). We will further explore how PHBA regulates the metabolic mechanism in blood after cerebral I/R to find an effective therapeutic target to prevent and treat IS. Firstly, using the rat model of cerebral ischemia-reperfusion injury induced by middle cerebral artery occlusion/Reperfusion (MCAO/R). The therapeutic effect of PHBA on brain I/R was evaluated by neurological function score, triphenyl tetrazolium chloride (TTC), Hematoxylin and eosin (HE), and Nissl staining. Secondly, a non-targeted metabonomic based on HPLC-QTOF-MS/MS was established to identify differential metabolites. Finally, we analyzed a targeted metabolic spectrum and verified the potential therapeutic targets. The results showed that the neurological function score, cerebral infarction area, hippocampal morphology, and the number of neurons in the PHBA group were significantly improved compared with the model group. Metabonomic analysis showed that 13 different metabolites were identified between the model and PHBA group, which may be involved in the 'tricarboxylic acid cycle', 'glutathione metabolism', 'mutual transformation of pentose and glucuronates', and so on. Among them, the most significant differential metabolite, dGMP, decreased significantly after PHBA treatment. We used WB to verify the expression of membrane-associated guanosine kinase PSD-95 and The subunit of glutamate AMPA receptor GluA1, which significantly increased after PHBA treatment. In addition, we also found that PHBA increased the expression of the light chain-3 protein (LC3) and autophagy effector protein 1 (Beline1) in WB while decreasing the expression of sequestosome-1 (p62), indicating that autophagy activity was promoted. Similarly, in TUNEL staining and detection of apoptosis-related proteins, it was found that MCAO/R up-regulated the expression of Bax and Cleaved-caspase-3 while down-regulated the expression of Bcl-2, and increased the apoptosis of hippocampal neurons, but PHBA could improve this situation. In summary, these results suggest that cerebral I/R causes postsynaptic dysfunction by disrupting the interaction between PSD-95 and AMPARs, and the inhibition of the autophagy system eventually leads to the apoptosis of hippocampal neurons.</p>
2024-07-04 | MTBLS7870 | MetaboLights
Project description:The ketogenic diet (KD) is used to treat a number of brain pathologies. In this study, we undertook detailed transcriptomic profiling of rat brain after KD and ischemic stroke to uncover effects of KD and its specific mechanisms. We evaluated how a 2-month KD affected gene expression in intact brain tissue and after middle cerebral artery occlusion (MCAO). We found transcriptional reprogramming in the brain after stroke and KD treatment. KD altered the expression of genes involved in the regulation of glucose and fatty acid metabolism, mitochondrial function, immune response, Wnt-associated signaling, stem cell development, and neurotransmission in both intact rats and after MCAO.
2024-10-11 | GSE272485 | GEO
Project description:To further delineate tPA functions in the blood, we examined the gene expression profiles induced by tPA in a rat model of ischemic stroke. Forty-two Sprague-Dawley rats were subjected to: 2 hours of middle cerebral artery occlusion (MCAO); a permanent-MCAO; or were used as controls. tPA was administered to half of the rats in each group at 3hours. Whole blood was drawn at 24 hours, and isolated RNA levels measured on Affymetrix Rat Genome 230 2.0 GeneChip microarrays to examine the entire RNA transcriptome. 42 samples, 7 groups in total ( 2 treatmented disease, 2 untreated disease, and 3 control groups), each group had 6 replicates
2014-03-29 | E-GEOD-21136 | biostudies-arrayexpress
Project description:To further delineate tPA functions in the blood, we examined the gene expression profiles induced by tPA in a rat model of ischemic stroke. Forty-two Sprague-Dawley rats were subjected to: 2 hours of middle cerebral artery occlusion (MCAO); a permanent-MCAO; or were used as controls. tPA was administered to half of the rats in each group at 3hours. Whole blood was drawn at 24 hours, and isolated RNA levels measured on Affymetrix Rat Genome 230 2.0 GeneChip microarrays to examine the entire RNA transcriptome.
2014-03-29 | GSE21136 | GEO
Project description:Posttranslational modifications with ubiquitin alter protein function and stability, thereby regulating cell homeostasis and viability, particularly under stress. Ischemic stroke induces protein ubiquitination at the periphery of the ischemic territory, wherein cells remain viable. Revealing the identity of ubiquitinated proteins, their cellular location, and the functional consequences of ubiquitin modification may shed light on the role of ubiquitination in ischemic injury. Here, we employed a proteomics approach to identify proteins ubiquitinated following ischemic stroke, induced by transient middle cerebral artery occlusion (tMCAO) in mice. We detected increased ubiquitination of 198 proteins, many of which localize to the postsynaptic density (PSD) of glutamatergic neurons. Among these were proteins essential for maintaining PSD architecture, such as PSD93, PSD95 and Shank3, as well as NMDA and AMPA receptor subunits. The largest enzymatic group at the PSD with high post-ischemic ubiquitination levels were kinases, such as CaMKII, PKC, Cdk5, and Pyk2, the aberrant activity of which contributes to post-ischemic neuronal death. Concurrent phospho-proteomics revealed altered phosphorylation patterns associated with the PSD, indicative of modified PSD kinase activity following stroke. CaMKII, PKC, and Cdk5 activity was decreased while Pyk2 activity was increased at the PSD after stroke, accompanied by the hypo- and hyper-phosphorylation of downstream targets, respectively. Removal of ubiquitin restored kinases’ activity to pre-stroke levels, identifying ubiquitination as the responsible molecular mechanism for post-ischemic kinase regulation. These findings unveil a previously unrecognized role of post-ischemic ubiquitination in the regulation of essential kinases involved in ischemic injury, and presents targeting ubiquitination as a potential new avenue for the treatment of ischemic stroke.
2023-09-06 | PXD042951 | Pride