Gene expression data from mouse brain endothelial cells after SAH
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ABSTRACT:
PROVIDER: PRJNA648765 | ENA |
REPOSITORIES: ENA
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Project description:SAH pathophysiology includes blood-brain barrier (BBB) disruption. Gene expression changes at the endothelial cell level may provide insight into BBB pathophysiology. We used microarray gene expression data comparing freshly isolated brain endothelial cells isolated from Sham or SAH mice.
2021-04-12 | GSE155137 | GEO
Project description:Using the SAH model to conduct experiments, set 5 groups of experimental groups and 5 groups of control groups. Studying the effects on the white matter cells of normal mice and the mice with SAH
2019-10-10 | E-MTAB-8407 | biostudies-arrayexpress
Project description:Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations. The working hypothesis was that endothelial cells which are actively building a barrier would have a uniqe pattern of gene expression that would be detectable in comparison to a non-barrier endothelial population that is also active in vasculogenesis.
2014-05-14 | GSE56777 | GEO
Project description:Elevated glucocorticoids feature body’s responses to a variety of psychological and physiological stressors. To understand how glucocorticoids affect brain endothelial cells that form the blood-brain barrier, we applied quantitative proteomics to study changes in the proteome of a mouse brain endothelial cell line, bEnd3, upon acute 24-hour treatment with 5 uM corticosterone in vitro.
2021-03-01 | PXD022166 | Pride
Project description:Following the identification of a critical time window of Blood Brain Barrier formation in the mouse embryo, we aimed to identify genes important for barriergenesis. To this end, we isolated cortical and lung E13.5 endothelial cells and compared expression between the two populations. The working hypothesis was that endothelial cells which are actively building a barrier would have a uniqe pattern of gene expression that would be detectable in comparison to a non-barrier endothelial population that is also active in vasculogenesis. E13.5 Tie2-GFP embryos were micro-dissected for cortex and lungs. Cortex tissue was carefully cleared of the meninges and choroid plexus. FACS purification of GFP positive cells and GeneChip analysis was applied . All material from a single litter (10-13 embryos) was pooled and considered as a biological replicate. n=4 litters.
2014-05-14 | E-GEOD-56777 | biostudies-arrayexpress
Project description:<p><strong>BACKGROUND:</strong> Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with a poor prognosis. Accumulating studies have reported that gut microbiota contributes to the pathophysiology of several central nervous system diseases. However, whether SAH can change gut microbiota composition and affected gut microbiota is involved in the development of secondary brain injury following SAH remains unclear.</p><p><strong>METHODS:</strong> A retrospective case-control study was performed in unruptured intracranial aneurysm (UIA, CTL) and ruptured intracranial aneurysm (SAH) patients. Patients' fecal and serum samples were collected and sequenced by metagenome and metabolome. The experimental SAH mice models were established, and their feces and serum were also analyzed by 16S rRNA and metabolic sequencing. Fecal microbiota from SAH patients and mice was transplanted to ABX mice to investigate the relationship between the gut microbiota and secondary brain injury following SAH.</p><p><strong>RESULTS:</strong> SAH seriously influenced gut microbiota composition and significantly increased the relative abundance of the genus Escherichia. SAH also considerably reduced the production of gut microbiota-derived butyric acid. Furthermore, SAH-induced gut microbiota dysbiosis aggravated brain injury and cognitive deficits in ABX mice by promoting inflammatory response. Sodium butyrate (NaB) administration protected against secondary brain injury following SAH by inhibiting pyroptosis-related neuroinflammation, which is mediated by NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME signaling pathways. NaB drinking pretreatment also alleviated secondary brain injury following SAH by increasing the relative abundance of butyric acid-producing bacteria, such as Dubosiella and Faecalibaculum, and decreasing the Escherichia abundance.</p><p><strong>CONCLUSION:</strong> SAH contributed to gut microbiota dysbiosis and changed gut microbiota exacerbated secondary brain injury after SAH. Supplement with gut microbiota-derived butyric acid protected against brain injury following SAH by inhibiting NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME-mediated neuronal pyroptosis.</p><p><br></p><p><strong>Linked studies:</strong></p><p><strong>UPLC-MS/MS</strong> assays of human samples are reported in this study.</p><p><strong>UPLC-MS/MS</strong> assays of murine samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS9100' rel='noopener noreferrer' target='_blank'><strong>MTBLS9100</strong></a>.</p>
2024-07-09 | MTBLS9087 | MetaboLights
Project description:<p><strong>BACKGROUND:</strong> Subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with a poor prognosis. Accumulating studies have reported that gut microbiota contributes to the pathophysiology of several central nervous system diseases. However, whether SAH can change gut microbiota composition and affected gut microbiota is involved in the development of secondary brain injury following SAH remains unclear.</p><p><strong>METHODS:</strong> A retrospective case-control study was performed in unruptured intracranial aneurysm (UIA, CTL) and ruptured intracranial aneurysm (SAH) patients. Patients' fecal and serum samples were collected and sequenced by metagenome and metabolome. The experimental SAH mice models were established, and their feces and serum were also analyzed by 16S rRNA and metabolic sequencing. Fecal microbiota from SAH patients and mice was transplanted to ABX mice to investigate the relationship between the gut microbiota and secondary brain injury following SAH.</p><p><strong>RESULTS:</strong> SAH seriously influenced gut microbiota composition and significantly increased the relative abundance of the genus Escherichia. SAH also considerably reduced the production of gut microbiota-derived butyric acid. Furthermore, SAH-induced gut microbiota dysbiosis aggravated brain injury and cognitive deficits in ABX mice by promoting inflammatory response. Sodium butyrate (NaB) administration protected against secondary brain injury following SAH by inhibiting pyroptosis-related neuroinflammation, which is mediated by NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME signaling pathways. NaB drinking pretreatment also alleviated secondary brain injury following SAH by increasing the relative abundance of butyric acid-producing bacteria, such as Dubosiella and Faecalibaculum, and decreasing the Escherichia abundance.</p><p><strong>CONCLUSION:</strong> SAH contributed to gut microbiota dysbiosis and changed gut microbiota exacerbated secondary brain injury after SAH. Supplement with gut microbiota-derived butyric acid protected against brain injury following SAH by inhibiting NLRP1/Caspase-1/GSDMD and Caspase-3/GSDME-mediated neuronal pyroptosis.</p><p><br></p><p><strong>Linked studies:</strong></p><p><strong>UPLC-MS/MS assays</strong> of murine samples are reported in this study.</p><p><strong>UPLC-MS/MS</strong> <strong>assays</strong> of human samples are reported in <a href='https://www.ebi.ac.uk/metabolights/MTBLS9087' rel='noopener noreferrer' target='_blank'><strong>MTBLS9087</strong></a>.</p>
2024-07-09 | MTBLS9100 | MetaboLights
Project description:Brain endothelial cells have specific characteristics that differentiate them from other vascular beds. We used transcriptomics of mouse and human brain endothelial cells to explore this differences.
2024-02-06 | GSE244349 | GEO
Project description:To understand the molecular mechanisms during the maturation of cord blood-derived endothelial cells into blood brain barrier capillary endothelial cells (BCECs), we have employed whole genome microarray expression profiling to identify genes responsible for the maturation process. Hematopoietic stem cells were isolated from cord-blood samples and differentiated into endothelial cells. The endothelial cells were further maturated into BCECs by co-culturing with blood-brain barrier (BBB) specific cells (pericytes) for 3 days and 6 days. The gene expression in human hematopoietic stem cell-derived endothelial cells was measured at 3 and 6 days after co-culture with pericytes. Three independent experiments were performed at each time (3 or 6 days). The RNA obtained from different experiments were pooled together for each group before microarray studies.
2013-10-18 | E-GEOD-45171 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) is a highly aggressive and vascularized malignant brain tumor. Anti-VEGF therapy is widely used for the treatment of GBM, however it has shown only minor impact on patient survival. Thus, more precise molecular mechanisms for glioma angiogenesis are needed for the advance in the treatment of GBM. Here, we investigated gene expression profile of brain endothelial cells and glioma endothelial cells using RNA sequencing to validated special molecular features of glioma endothelial cells.
2017-11-24 | GSE90459 | GEO