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Gene expression in commercial human cerebral microvascular endothelial cells (hCMECs) line knock out or not for RNF213

ABSTRACT: To study the role of RNF213, we generated RNF213-deficient human cerebral microvascular endothelial cells by the CRISPR-Cas9 double nickase method and showed that RNF213 may be an important regulator of the blood-brain barrier permeability and homeostasis

ORGANISM(S): Homo sapiens

PROVIDER: GSE183603 | GEO | 2021/09/08

REPOSITORIES: GEO

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Gene expression in commercial human cerebral microvascular endothelial cells (hCMECs) line knock out or not for RNF213

Project description:Gene expression in commercial human cerebral microvascular endothelial cells (hCMECs) line knock out or not for RNF213

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RNA-seq of induced brain microvascular endothelial cells from cerebral childhood adrenoleukodystrophy patients and wild-type controls

Project description:The goal of this study is to compare gene expression differences between induced brain microvascular endothelial cells from cerebral childhood adrenoleukodystrophy patients and wild-type controls

2018-04-01 | GSE108012 | GEO

Marinobufagenin regulates gene expression in human brain microvascular endothelial cells in vitro.

2013-11-01 | GSE51351 | GEO

Systemic and cerebral iron homeostasis in ferritin knock-out mice.

Project description: Not available

| S-EPMC4309591 | biostudies-literature

Ultra-Processed Foods drive Intestinal Barrier permeability increasing Microvascular Disease risk

Project description:Ultra-Processed Foods drive Intestinal Barrier permeability increasing Microvascular Disease risk

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Incidence of microvascular dysfunction is increased in hyperlipidemic mice, reducing cerebral blood flow and impairing remote memory.

Project description:The development of cognitive dysfunction is not necessarily associated with diet-induced obesity. We hypothesized that cognitive dysfunction might require additional vascular damage, for example, in atherosclerotic mice. We induced atherosclerosis in male C57BL/6N mice by injecting AAV-PCSK9DY (2x1011 VG) and feeding them a cholesterol-rich Western diet. After 3 months, mice were examined for cognition using Barnes maze procedure and for cerebral blood flow. Cerebral vascular morphology was examined by immunehistology. In AAV-PCSK9DY-treated mice, plaque burden, plasma cholesterol, and triglycerides are elevated. RNAseq analyses followed by KEGG annotation show increased expression of genes linked to inflammatory processes in the aortas of these mice. In AAV-PCSK9DY-treated mice learning was delayed and long-term memory impaired. Blood flow was reduced in the cingulate cortex (-17%), caudate putamen (-15%), and hippocampus (-10%). Immunohistological studies also show an increased incidence of string vessels and pericytes (CD31/Col IV staining) in the hippocampus accompanied by patchy blood-brain barrier leaks (IgG staining) and increased macrophage infiltrations (CD68 staining). We conclude that the hyperlipidemic PCSK9DY mouse model can serve as an appropriate approach to induce microvascular dysfunction that leads to reduced blood flow in the hippocampus, which could explain the cognitive dysfunction in these mice.

2024-02-26 | GSE247400 | GEO

Marinobufagenin regulates gene expression in human brain microvascular endothelial cells in vitro.

Project description:To understand the mechanism by which MBG increases permeability of human brain microvascular endothelial cell (HBMEC) monolayers, the primary cultures were treated with 10nM MBG for 12 h. RNA was isolated and analysed for gene expression on Agilent one color microarrays. Triplicate wells of HBMEC were treated with 10 nM MBG in DMSO or with just the drug vehicle for 12 h. RNA was isolated from each well and used to reverse transcribe and generate Cy3-labelled cRNA. Microarrays were hybridized, washed and scanned. Data were normalized and assessed for differential gene expression between MBG treated and control HBMEC.

2013-11-01 | E-GEOD-51351 | biostudies-arrayexpress

Comparative genomic profile of human brain microvascular endothelial cells upon TWEAK or TNFα stimulation at 3h, 12h, and 24h

Project description:The molecular mechanisms playing a role in TWEAK versus TNFɑ signaling on cerebral microvascular endothelial cells are not well defined. Therefore, we aimed to identify gene expression changes in cultures of human brain microvascular endothelial cells (hCMEC/D3) to address changes initiated by TWEAK exposure. Although related, these two cytokines mediated different effects on gene expression and on canonical pathway activation. We used Agilent Whole Human Genome Microarray 4X44K to compare TWEAK- and TNFɑ-mediated changes in gene expression after 3h, 12h, and 24h incubation of these cytokines.

2022-10-20 | E-MTAB-12222 | biostudies-arrayexpress

Thrombospondin1 replacement prevents cerebral cavernos malformations

Project description:We have purified primary brain microvascular endothelial cells (BMEC) from mice bearing floxed alleles of Krit1 (Krit1fl/fl) and an endothelial specific tamoxifen-regulated Cre recombinase (Pdgfb-iCreERT2), and used these to delete Krit1 in a time-controlled manner (Krit1ECKO). To elucidate the pathogenesis of cerebral cavernous malformations (CCM) we used genome-wide RNA sequencing (RNA-seq) to characterize the transcriptome of primary BMEC following acute genetic inactivation of Krit1.

2017-09-25 | GSE85657 | GEO

Acid sphingomyelinase deactivation post-ischemia/ reperfusion promotes cerebral angiogenesis and brain remodeling via small extracellular vesiclesAcid sphingomyelinase deactivation post-ischemia/ reperfusion promotes cerebral angiogenesis and brain remodeling via small extracellular vesicles

Project description:Acid sphingomyelinase (ASM) inhibitors, which are clinically used as anti-depressants for ~60 years, have recently been shown to enhance stroke recovery in rodents. Using mice and cerebral microvascular endothelial cells exposed to ischemia/reperfusion (I/R) we show that the antidepressants amitriptyline, fluoxetine and desipramine induce angiogenesis in an ASM-dependent way by releasing small extracellular vesicles (sEVs) from endothelial cells, which have bona fide characteristics of exosomes and which, similar to sEVs released during I/R, promote angiogenesis. Post-I/R, ASM inhibition elicits a profound brain remodeling response with increased blood-brain barrier integrity, reduced brain leukocyte infiltrates and increased neuronal survival. The ASM inhibitor-mediated release of sEVs has disclosed an elegant target, via which stroke recovery can be amplified. Key words: Antidepressant, ceramide, exosome, focal cerebral ischemia, middle cerebral artery occlusion, sphingomyelin, stroke recovery

2022-10-14 | PXD024106 | Pride

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