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Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

ABSTRACT: Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

PROVIDER: PRJNA1032618 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26537809_1.fastq.gz	Fastqsanger.gz
	SRR26537809_2.fastq.gz	Fastqsanger.gz
	SRR26537810_1.fastq.gz	Fastqsanger.gz
	SRR26537810_2.fastq.gz	Fastqsanger.gz
	SRR26537811_1.fastq.gz	Fastqsanger.gz

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Inflammation and neutrophil extracellular traps in cerebral cavernous malformation

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Project description:Cerebral cavernous malformations are vascular anomalies that can cause hemorrhagic stroke. Mutations in genes encoding Krit 1 (CCM1), OSM (CCM2), and PDCD10 (CCM3) proteins cause CCM. A loss in teh expression of any of these CCM proteins disrupts normal cerebral vessel development by disrupting the cytoskeleton and thereby inhibits endothelial tube ofrmation. Examination of cellular changes based on the loss of CCM gene expression may lead to the methods for early detection and prevention of CCM associated hemorrhagic stroke.

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Project description:Cerebral Cavernous Malformation (CCM) is a brain vascular disease with various neurological symptoms. In this study, we describe the inflammatory profile in CCM and show for the first time the formation of neutrophil extracellular traps (NETs) in rodents and humans with CCM. Through RNA-seq analysis of cerebellum endothelial cells from wild-type mice and mice with an endothelial cell-specific ablation of the Ccm3 gene (Ccm3iECKO), we show that endothelial cells from Ccm3iECKO mice have an increased expression of inflammation-related genes. These genes encode proinflammatory cytokines and chemokines, as well as adhesion molecules, which promote recruitment of inflammatory and immune cells. Similarly, immunoassays showed elevated levels of these cytokines and chemokines in the cerebellum of the Ccm3iECKO mice. Consistently, both flow cytometry and immunofluorescence analysis showed infiltration of different subsets of leukocytes into the CCM lesions. Neutrophils, which are known to fight against infection through different strategies, including the formation of NETs, represented the leukocyte subset within the most pronounced increase in CCM. Here, we detected elevated levels of NETs in the blood and the deposition of NETs in the cerebral cavernomas of Ccm3iECKO mice. Degradation of NETs by DNase I treatment improved the vascular barrier. The deposition of NETs in the cavernomas of patients with CCM confirms the clinical relevance of NETs in CCM.

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Comprehensive Transcriptome Analysis of Cerebral Cavernous Malformation Across Multiple Species and Genotypes

Project description:Purpose: To determine important genes, functions, and networks contributing to the pathobiology of cerebral cavernous malformation (CCM) from transcriptomic analyses across 3 species and 2 disease genotypes. Methods: Sequencing of RNA from laser microdissected neurovascular units (NVUs) of 5 human surgically resected CCM lesions, mouse brain microvascular ECs (BMECs) and C. elegans with induced Ccm gene loss, and their respective controls, provided differentially expressed genes (DEGs). DEGs from mouse and C. elegans were annotated into human homologous genes. Cross-comparisons of DEGs between species and genotypes as well as network and Gene Ontology (GO) enrichment analyses were performed. Results: Among hundreds of DEGs identified in each model, common genes and one GO term (GO:0051656 establishment of organelle localization) were commonly identified across the different species and genotypes. In addition, 24 GO functions were present in 4 out of 5 models and were related to cell-cell adhesion, neutrophil mediated immunity, ion transmembrane transporter activity, and responses to oxidative stress. We provide a comprehensive transcriptome library of CCM disease across species, and for the first time in Ccm1/Krit1 versus Ccm3/Pdcd10 genotypes Conclusion: We provide examples of how results can be used in hypothesis generation or mechanistic confirmatory studies.

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Specific post-translational histone mod. of neutrophil extracellular traps as immunogens & potential SLE Ab targets.

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