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Hypoxia increases neuroinflammation and angiogenesis gene programs in CCM disease

ABSTRACT: Hypoxia increases neuroinflammation and angiogenesis gene programs in CCM disease

PROVIDER: PRJNA989155 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25074059_1.fastq.gz	Fastqsanger.gz
	SRR25074059_2.fastq.gz	Fastqsanger.gz
	SRR25074060_1.fastq.gz	Fastqsanger.gz
	SRR25074060_2.fastq.gz	Fastqsanger.gz
	SRR25074061_1.fastq.gz	Fastqsanger.gz

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Hypoxia increases neuroinflammation and angiogenesis gene programs in CCM disease

2024-09-23 | GSE236163 | GEO

Reactive astrocytes with inflammatory signature in CCM disease in hypoxia and normoxia conditions

Project description:The CCM endothelium is hypersensitive to angiogenesis and can induce a hypoxic program associated with changes in angiogenesis, inflammation, and endothelial-cell metabolism under normoxic conditions. However, the role of active drivers of angiogenesis as CCM disease modifiers in human disease remains unclear. To assess whether CCM reactive astrocytes with neuroinflammatory capacity respond to hypoxia-induced CCM exacerbation, we employed the astrocyte-specific (Aldh1l1-EGFP/Rpl10a) Translational Ribosome Affinity Purification (TRAP) system in combination with a CCM mouse model (Pdcd10BECKO;Aldh1l1-EGFP/Rpl10a). TRAP protocol was performed using Slco1c1-iCreERT2;Pdcd10fl/fl;Aldh1l1-EGFP/Rpl10a mice to isolate ribosomes from astrocytes as previously described. Astrocyte-TRAP mRNAs were from cerebral tissue of mice age P50 exposed to hypoxia or normoxia conditions.

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Neuroinflammation and immunothrombosis transcriptional patterns in CCM lesions revealed by spatial transcriptomics

Project description:Cerebral cavernous malformation (CCM) immunothrombosis is the connection between immune cells, platelet activation, coagulation cascades and astrocyte-CCM endothelium interaction, and its excessive activation may contribute to neurological disabilities in CCM disease. We characterized the spatial organization of CCM immunothrombosis observed in Pdcd10BECKObrains under normoxic conditions using the murine 10X Genomics Visium Spatial Gene Expression platform.

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Neuroinflammation and immunothrombosis transcriptional patterns in CCM lesions revealed by spatial transcriptomics

Project description:Neuroinflammation and immunothrombosis transcriptional patterns in CCM lesions revealed by spatial transcriptomics

| PRJNA989154 | ENA

Gene expression changes in LPS-induced neuroinflammation

Project description:Neuroinflammation plays a role in the progression of several neurodegenerative disorders. We used a lipolysaccharide (LPS) model of neuroinflammation to characterize the gene expression changes underlying the inflammatory and behavioral effects of neuroinflammation. A single intracerebroventricular injection of LPS (5 ug) was administered into the lateral ventricle of mice and, 24 hours later, we examined gene expression in the cerebral cortex and hippocampus using microarray technology. Gene Ontology (GO) terms for inflammation and the ribosome were significantly enriched by LPS, whereas GO terms associated with learning and memory had decreased expression. We detected 224 changed transcripts in the cerebral cortex and 170 in the hippocampus. Expression of Egr1 (also known as Zif268) and Arc, two genes associated with learning and memory, was significantly lower in the cortex, but not hippocampus, of LPS-treated animals. Overall, altered expression of these genes may underlie some of the inflammatory and behavioral effects of neuroinflammation. Mice were given intracerebroventricular injections of saline vehicle (n = 4) or lipopolysaccharide (n = 4). Twenty-four hours later, we dissected the hippocampus and cerebral cortex and processed the tissue for microarray analysis. Gene expression changes observed in the microaray data were validated with quantitative real-time PCR.

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mTORC1 signaling in brain endothelial progenitors contributes to CCM pathogenesis in a Pdcd10-deficient mouse model

Project description:Cerebral vascular malformations (CCM) are primarily found within brain, where they result in increased risk for stroke, seizures and focal neurological deficits. The unique feature of the brain vasculature is the blood-brain barrier (BBB) formed by the brain neurovascular unit, and recent studies suggest that loss of CCM genes causes disruptions of BBB integrity as the inciting event for the development of CCM. CCM lesion is proposed to be initially derived from a single clonal expansion of a subset of angiogenic venous capillary endothelial cells (ECs) and respective resident endothelial progenitor cells (EPCs). However, the critical signaling in the subclass of brain EC/EPC for the CCM lesion initiation and progression are unclear. Here we employed single-cell RNA-sequencing (scRNA-seq) analyses in early stages of the brain EC-specific Ccm3 deletion (Pdcd10BECKO) microvessels and identified a unique EPC cluster with high stem cell markers but low BBB-associated genes. mTORC1, but not mTORC2, is activated in mouse and human CCM lesions and EPCs. Mechanistic studies suggest that CCM3 suppresses Cav1/caveolae-mediated cellular trafficking and complex formation of the mTORC1 signaling proteins. Genetic deficiency of Raptor (mTORC1), but not of Rictor (mTORC2), prevents CCM lesion formation in the Pdcd10BECKO model. Importantly, mTORC1 pharmacological inhibitor Rapamycin ameliorate the CCM pathogenesis in the Pdcd10BECKO mice, by suppressing lesion-forming EPC expansion while enhancing BBB maturation. Our data suggest that CCM3 is critical for maintaining BBB integrity, and CCM3 loss-induced mTORC1 signaling in brain EPCs initiate the CCM pathogenesis.

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2020-05-26 | PXD014019 | Pride

Perivascular B cells link intestinal angiogenesis to immunity and to the gut-brain axis during neuroinflammation

Project description:Perivascular B cells link intestinal angiogenesis to immunity and to the gut-brain axis during neuroinflammation

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Perivascular B cells link intestinal angiogenesis to immunity and to the gut-brain axis during neuroinflammation

Project description:Disruption of gut barrier function and intestinal immune cell homeostasis are increasingly considered critical players in pathogenesis of extra-intestinal inflammatory diseases, including multiple sclerosis (MS) and its prototypical animal model, theexperimental autoimmune encephalomyelitis (EAE). Breakdown of epithelial barriers increases intestinal permeability and systemic dissemination of microbiota-derived molecules. However,whetherthe gut-vascular barrier (GVB) is altered during EAE has not been reported. Here, we demonstrate that endothelial cell proliferation and vessel permeability increase before EAE clinical onset, leadingto vascular remodelingand expansion of intestinal villi capillary bed during disease symptomatic phasein an antigen-independent manner. Concomitant to onset of angiogenesis observed prior to neurological symptoms, we identify an increase of intestinal perivascular immune cells characterized by the surface markerlymphatic vessel endothelial hyaluronic acid receptor 1 (LYVE-1). LYVE-1+is expressed more frequently on B cells that show high levels of CD73 and have proangiogenic properties. B cell depletion was sufficient tomitigate enteric blood endothelial cell proliferation following immunization for EAE. In conclusion, we propose that altered intestinal vasculature driven by a specialized LYVE-1+B cell subset promotes angiogenesis and that loss of GVB function is implicated in EAE development and autoimmunity.

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