To explore the changes in the genes expression profile between brain and skull after ischemic injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA789942 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17267035_1.fastq.gz | Fastqsanger.gz | |||
| SRR17267035_2.fastq.gz | Fastqsanger.gz | |||
| SRR17267036_1.fastq.gz | Fastqsanger.gz | |||
| SRR17267036_2.fastq.gz | Fastqsanger.gz | |||
| SRR17267037_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:We longitudinally monitor the cortical/calvarial vascular injury and regeneration processes after ischemic injury in awake mice. Results show that calvarial blood vessels recover earlier than the cortex. Further, by transcriptome analysis, we finds gene expression patterns and immune cells abundances exist great differences between brain and skull after ischemic injury, which may be one of the causes for the time lag between their vascular recovery. These findings bring great enlightenment to the vascular regeneration and reconstruction.
2021-12-20 | GSE191183 | GEO
Project description:Background: Previous study showed that stroke may be a potential first sign of neoplasia. But the relationship between them remains unclear. Besides, ischemic stroke is a complex brain disease, which involves cell death or complex immune regulation. Thus, it is necessary to reveal the association of tumor immune microenvironment and cell death with ischemic stroke. Methods: Here, a photothrombosis-induced ischemic injury models of brain and skull was established. We compared and analyzed the pattern of gene expression profile between brain and skull after ischemic injury by transcriptome analysis. Further, we investigated the enrichment of relevant differential genes in cancer pathways and cell death pathways, and analyzed changes in the immune microenvironment after ischemic injury. Moreover, the pan-cancer genomic and prognosis analysis of ischemic injury related gene set were performed. Results: The results showed that the gene expression patterns were different in temporal and spatial locations after ischemic injury. We found that the effect on the transcriptome of the brain after skull ischemic injury was particularly large, but it could be recovered in a short period, while the effect on the skull after brain ischemic injury was long-lasting. The expression of genes related to ischemic injury is also associated with cell death and cancer hallmark pathways. In addition, changes in the abundance of immune cells indicate that brain ischemic injury may disrupt its immune microenvironment for a longer time, while skull can better balance the stability of immune microenvironment. Moreover, the brain ischemic injury-related gene sets are highly correlated with a variety of tumors, especially GBM, KIRC, LGG and UVM after stroke have a greater risk of death. Conclusion: This study gives us a new understanding of the role of the skull in brain ischemic injury, and reveals the association of tumor immune microenvironment and cell death with ischemic stroke.
2022-09-25 | GSE213429 | GEO
Project description:Stroke involves in the interaction between central and peripheral immune systems. Skull bone marrows serve as reservoirs for immune cells in brain borders, and can rapidly respond to perturbations in the brain environment. Hence, targeting the skull bone marrow to modulate neuroimmune communications along the calvaria-meninges-brain axis would potentially improve stroke prognosis. Here, we successfully achieved cranial immunomodulation via ultraviolet (UV) irradiation of the interparietal region, which was characterized by rich marrow cavities and channels connecting the skull and meninges. Utilizing the recently-developed long-term clearing cranial window that ensured the integrity of skull, we discovered that the cranial photo-immunologic regulation (CPR) could promote cerebrovascular regeneration and aid in neurovascular repair post ischemic stroke. Single-cell transcriptome analysis revealed that meninge could be a crucial neuroimmune interface for ischemic stroke-induced immune responses. And, CPR could restore the stroke-induced alterations in cellular gene expression, especially meningeal B cells. Further we demonstrated that CPR could effectively alleviate the excessive suppression of meningeal B cell activation caused by ischemic stroke. This work opens avenues for immunoregulation through the skull-meninges-brain axis and provides valuable insights for immunomodulatory therapies in brain diseases.
2024-04-18 | GSE254550 | GEO
Project description:Stroke involves in the interaction between central and peripheral immune systems. Skull bone marrows serve as reservoirs for immune cells in brain borders, and can rapidly respond to perturbations in the brain environment. Hence, targeting the skull bone marrow to modulate neuroimmune communications along the calvaria-meninges-brain axis would potentially improve stroke prognosis. Here, we successfully achieved cranial immunomodulation via ultraviolet (UV) irradiation of the interparietal region, which was characterized by rich marrow cavities and channels connecting the skull and meninges. Utilizing the recently-developed long-term clearing cranial window that ensured the integrity of skull, we discovered that the cranial photo-immunologic regulation (CPR) could promote cerebrovascular regeneration and aid in neurovascular repair post ischemic stroke. Single-cell transcriptome analysis revealed that meninge could be a crucial neuroimmune interface for ischemic stroke-induced immune responses. And, CPR could restore the stroke-induced alterations in cellular gene expression, especially meningeal B cells. Further we demonstrated that CPR could effectively alleviate the excessive suppression of meningeal B cell activation caused by ischemic stroke. This work opens avenues for immunoregulation through the skull-meninges-brain axis and provides valuable insights for immunomodulatory therapies in brain diseases.
2024-04-18 | GSE252774 | GEO
Project description:Cranial photo-immunologic regulation along the skull-meninges-brain axis for promoting recovery from ischemic brain injury
| PRJNA1071029 | ENA
Project description:Cranial photo-immunologic regulation along the skull-meninges-brain axis for promoting recovery from ischemic brain injury
| PRJNA1062428 | ENA
Project description:Systematic analysis of brain and skull ischemic injury expression profile reveals associations of tumor immune microenvironment and cell death with ischemic stroke
| PRJNA880635 | ENA
Project description:Epigenetic modifications, such as cytosine methylation and histone modification, have been shown involved in the pathology of ischemic brain injury. Recent works have implicated 5-hydroxymethylcytosine (5hmC), a DNA base derived from 5-methylcytosine (5mC) through the oxidation by Ten-Eleven Translocation (TET) enzymes, in DNA methylation-related plasticity. In this study we show that 5hmC abundance could be induced to increase by ischemia injury. Genome-wide profiling of 5hmC identified differentially hydroxymethylated regions (DhMRs) associated with ischemic injury and DhMRs were found enriched among the genes involved in cell junction, neuronal morphogenesis and neurodevelopment. These data together suggest that 5hmC modification could serve as a potential therapeutic target for the treatment of ischemic stroke. To determine the genome-wide 5hmC distribution in both ischemic injury (I/R) and control mice (C57BL/6), we employed a previously established chemical labeling and affinity purification method, coupled with high-throughput sequencing (Song et al, Nature Biotechnology, 2011). The ischemic or matched control brain tissues from three pairs of ischemic mice and control mice were used for the analyses.
2015-09-08 | E-GEOD-67188 | biostudies-arrayexpress
Project description:Microglia are resident CNS immune cells that are active sensors in healthy brain and versatile effectors under pathological conditions. Cerebral ischemia induces a robust neuroinflammatory response that includes marked changes in the gene expression and phenotypic profile of a variety of endogenous CNS cell types (astrocytes, neurons, microglia) as well as an influx of leukocytic cells (neutrophils, macrophages, T-cells) from the periphery. Many molecules and conditions can trigger a transformation of ârestingâ (or surveying) microglia to an âactivatedâ (alerted/reactive) state. Here we review recent developments in the literature that relate to microglial activation in the experimental setting of in vitro and in vivo ischemia. We also present new data from our own laboratory demonstrating the direct effects of in vitro ischemic conditions on the microglial phenotype and genomic profile. Emphasis is placed on the role of specific molecular signaling systems such as hypoxia inducible factor-1 (HIF-1) and toll-like receptor-4 (TLR4) in regulating the microglial response in this setting. We then review histological and recent novel radiological data that confirms a key role for microglial activation in the setting of ischemic stroke in humans. We discuss recent progress in the pharmacological and molecular targeting of microglia in acute ischemic stroke. Finally, we explore how recent studies on ischemic preconditioning have increased interest in preemptively targeting microglial activation in order to reduce stroke severity. 12 arrays, 4 experimental groups, 3 replicates in each group, CN is control normoxia, CH is control hypoxia, TN is TLR4 knockout normoxia, TH is TLR4 knockout hypoxia.
2010-10-05 | E-GEOD-18602 | biostudies-arrayexpress
Project description:Microglia are resident CNS immune cells that are active sensors in healthy brain and versatile effectors under pathological conditions. Cerebral ischemia induces a robust neuroinflammatory response that includes marked changes in the gene expression and phenotypic profile of a variety of endogenous CNS cell types (astrocytes, neurons, microglia) as well as an influx of leukocytic cells (neutrophils, macrophages, T-cells) from the periphery. Many molecules and conditions can trigger a transformation of “resting” (or surveying) microglia to an “activated” (alerted/reactive) state. Here we review recent developments in the literature that relate to microglial activation in the experimental setting of in vitro and in vivo ischemia. We also present new data from our own laboratory demonstrating the direct effects of in vitro ischemic conditions on the microglial phenotype and genomic profile. Emphasis is placed on the role of specific molecular signaling systems such as hypoxia inducible factor-1 (HIF-1) and toll-like receptor-4 (TLR4) in regulating the microglial response in this setting. We then review histological and recent novel radiological data that confirms a key role for microglial activation in the setting of ischemic stroke in humans. We discuss recent progress in the pharmacological and molecular targeting of microglia in acute ischemic stroke. Finally, we explore how recent studies on ischemic preconditioning have increased interest in preemptively targeting microglial activation in order to reduce stroke severity.
2010-10-05 | GSE18602 | GEO