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Transcriptomic analysis in cerebral microvessels from the brain of endothelial-specific Crif1 deficiency mouse

ABSTRACT: Transcriptomic analysis in cerebral microvessels from the brain of endothelial-specific Crif1 deficiency mouse

PROVIDER: PRJNA853747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19884814_1.fastq.gz	Fastqsanger.gz
	SRR19884814_2.fastq.gz	Fastqsanger.gz
	SRR19884815_1.fastq.gz	Fastqsanger.gz
	SRR19884815_2.fastq.gz	Fastqsanger.gz
	SRR19884816_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis in cerebral microvessels from the brain of endothelial-specific Crif1 deficiency mouse

Project description:Endothelial cells (ECs) in cerebral vessels are considered the primary targets in acute hemorrhagic brain injuries. EC dysfunction can aggravate neuronal injuries by causing secondary inflammatory responses and blood-brain barrier (BBB) disruption. ECs comprising the BBB are known to have a higher mitochondrial volume compared with peripheral ECs. In previous study, we reported Tek-CRIF1-knockout (KO) mice, with EC-specific deletion of the mitochondrial OxPhos-related gene, Crif1, also known as Gadd45gip1 (encoding GADD45G-interacting protein 1), display profound BBB defects accompanied by reduced expression of junctional proteins in ECs. To identify signaling pathways involved in linking EC-specific mitochondrial dysfunction and BBB disruption, we first performed RNA sequencing using isolated cerebral vessels from Tek-CRIF1 mice. This transcriptome analyses of the Tek-CRIF1-KO mouse revealed significant changes in some signaling, a pathway intimately involved in BBB maintenance.

2022-08-31 | GSE207106 | GEO

Stroke-induced transcriptomic alterations in mouse cerebral microvessels

Project description:To investigate the stroke-induced changes in gene expression in cerebral microvessels, we subjected mice to transient middle cerebral artery occlusion (tMCAO) or sham surgeries. 24h hours later, cerebral microvessels were harvested and RNA was isolated. We then performed gene expression profiling analysis using data obtained from RNA-seq of cerebral microvessels isolated from 8 mice (4 shams and 4 tMCAO)

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Mitochondrial regulator CRIF1 deficiency induces Foxp3low inflammatory non-suppressive regulatory-T cells in tumors [ATAC-seq]

Project description:Foxp3low inflammatory non-suppressive (INS)-regulatory T cells (Tregs) were discovered recently. Unlike conventional Tregs, they produce proinflammatory-cytokines, exhibit reduced suppressiveness, and promote rather than impair anti-tumor immunity. The role of mitochondria in Foxp3low INS-Treg formation in vivo is unclear. We showed that the Foxp3low INS-Treg equivalents in human tumors demonstrate attenuated expression of CRIF1, a vital mitochondrial regulator. Mice with CRIF1 deficiency in Tregs bore Foxp3low INS-Tregs with mitochondrial dysfunction. The -ketoglutarate-mTORC1 axis was enhanced in these cells. This promoted proinflammatory-cytokine expression by inducing EOMES and SATB1 expression. Moreover, chromatin openness of the regulatory regions of the Ifng and Il4 genes was increased, which facilitated EOMES/SATB1 binding. The increased -ketoglutarate-derived 2-hydroxyglutarate downregulated Foxp3 expression by methylating the Foxp3-gene regulatory regions. Furthermore, CRIF1-deficiency-induced Foxp3low INS-Tregs suppressed tumor growth in an IFN- dependent manner. Thus, CRIF1-mediated mitochondrial homeostasis is critical for inducing Foxp3low INS-Tregs that promote anti-tumor immunity.

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Project description:Stroke-induced transcriptomic alterations in mouse cerebral microvessels

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Project description:A filtration method followed by microarray analyses allows PDE components to be identified in brain microvessels, and confirmed that PDE4D and PDE5A are the primary forms expressed in rat brain microvessels. Adult male F344 rats were sacrificed and blocks of the cerebral cortex and infratentorial areas were dissected. Microvessels were isolated using a filtration method, and total RNA was extracted. Two microarrays using four sample RNAs (microvessels from the cerebral cortex vs. microvessels from the infratentorial block) were included in the present study. Microarrays demonstrated that there were 16 PDE transcripts in the PDE superfamily, exhibiting quantifiable density in the microvessels.

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β cell specific Crif1 haploinsufficiency effect.

Project description:CRIF1 is a mitochondrial protein essential for the synthesis and formation of the OxPhos complex in the inner mitochondrial membrane. Beta cell specific Crif1 haploinsufficiency resulted in defect of first phase insulin secretion, and caused islet cell composition change as well as proliferation of beta cell for a compensation to maintain metabolic homeostasis. These results suggest that mitochondrial OxPhos function of beta cell has roles for beta cell compensation as well as insulin secretion.

2022-07-21 | GSE151708 | GEO

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