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

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

PROVIDER: PRJNA761392 | ENA |

REPOSITORIES: ENA

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

Project description: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

2021-09-08 | GSE183603 | GEO

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

Expression data from Adam10 knock out mice and wild type

Project description:Adam10, a cell surface protease, cleaving many proteins including TNF-alpha and E-cadherin. Here we investigate the genome wide effects of Adam10 knock out on the transcriptome. Commercial microarrays (Affymetrix Mouse Gene ST 1.0) were used to generate genome wide mRNA profiles.

2011-01-06 | GSE25480 | GEO

Effects of Smoldering Eucalyptus Wood Smoke Extract on Primary Human Brain Microvascular Endothelial Cells (HBMEC) and Immortalized Human Cerebral Microvascular Endothelial Cell Line (hCMEC/D3)

Project description:Increase in frequency and size of wildfire raises a significant public health concern due to rapid climate change. Epidemiological studies have shown that wildfire smoke exposure can increase the risk of neurological disorders. Our study aims to understand how wildfire smoke particles affect brain endothelial cells using both primary human brain microvascular endothelial cells (HBMEC) and an immortalized human cerebral microvascular endothelial cell line (hCMEC/D3). HBMEC and hCMEC/D3 were exposed to different levels of smoldering eucalyptus smoke particles (10, 30, 50 ug/mL) for 24 hr. Supernatants were collected for LDH and ELISA array, cell lysates were collected for RNAseq, and cells were fixed and stained for tight junction marker (Zonula Occludens-1, ZO-1) via ICC. Our study found that treatment to smoldering eucalyptus particles can increase inflammatory cytokine production dose-dependently in HBMECs and hCMEC/D3. Moreover, RNAseq analyses resulted in dose-dependent changes in HBMEC and hCMEC/D3 from wood smoke treatment that could be mediated via AhR and Nrf2 pathways.

2024-10-02 | GSE271935 | GEO

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

Project description:Ferritin, a 24-mer heteropolymer of heavy (H) and light (L) subunits, is the main cellular iron storage protein and plays a pivotal role in iron homeostasis by modulating free iron levels thus reducing radical-mediated damage. The H subunit has ferroxidase activity (converting Fe(II) to Fe(III)), while the L subunit promotes iron nucleation and increases ferritin stability. Previous studies on the H gene (Fth) in mice have shown that complete inactivation of Fth is lethal during embryonic development, without ability to compensate by the L subunit. In humans, homozygous loss of the L gene (FTL) is associated with generalized seizure and atypical restless leg syndrome, while mutations in FTL cause a form of neurodegeneration with brain iron accumulation. Here we generated mice with genetic ablation of the Fth and Ftl genes. As previously reported, homozygous loss of the Fth allele on a wild-type Ftl background was embryonic lethal, whereas knock-out of the Ftl allele (Ftl-/-) led to a significant decrease in the percentage of Ftl-/- newborn mice. Analysis of Ftl-/- mice revealed systemic and brain iron dyshomeostasis, without any noticeable signs of neurodegeneration. Our findings indicate that expression of the H subunit can rescue the loss of the L subunit and that H ferritin homopolymers have the capacity to sequester iron in vivo. We also observed that a single allele expressing the H subunit is not sufficient for survival when both alleles encoding the L subunit are absent, suggesting the need of some degree of complementation between the subunits as well as a dosage effect.

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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.

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Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of control, SETD6 Knock-out, SETD3 knock-out and SETD6+SETD3 knock-out HeLa cells Transcriptomes

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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

aerobic knock-out

Project description:Six different knock-out strains' expression data under aerobic condition Keywords: parallel sample

2004-03-10 | GSE1106 | GEO

anaerobic knock-out

Project description:Six different knock-out strains' expression data under anaerobic condition Keywords: parallel sample

2004-03-10 | GSE1107 | GEO