Gene expression data from mouse brain endothelial cells after SAH
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE155137 | GEO | 2021/04/12
REPOSITORIES: GEO
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Project description:Gene expression data from mouse brain endothelial cells after SAH
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Project description:The blood-brain barrier (BBB) represents a major challenge when developing central nervous system (CNS)-active therapeutics. The non-human primate (NHP)-brain endothelium constitutes an essential alternative to human in the prediction of molecule trafficking across the BBB and in the search of new brain-specific transport mechanisms. This study presents a comparison between the NHP transcriptome of freshly isolated brain microcapillaries and in vitro-selected brain endothelial cells (BECs), focusing on important BBB features – tight junctions, receptors mediating transcytosis (RMT), ABC and SLC transporters. In vitro BECs conserved most of the BBB key elements for barrier integrity and control of molecular trafficking. We also assessed the function of RMT via the Transferrin Receptor (TFRC) in the characterized NHP-BBB model, where both human transferrin and anti-hTFRC antibody showed increased apical-to-basolateral passage in comparison to control molecules. In parallel, we investigated eventual BBB-related regional differences in 7-day in vitro-selected BECs from 5 brain structures: brainstem, cerebellum, cortex, hippocampus and striatum. Our analysis retrieved very few differences in the brain endothelium from these 5 brain regions, suggesting a rather homogeneous BBB role and function across the brain parenchyma. In conclusion, the presently established NHP-derived BBB model closely mimics the physiological BBB, therefore representing a ready-to-use tool for assessment of the penetration of biotherapeutics into the human CNS.
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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>
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