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Gene expression profile in HCAECs transfected with RNF213 siRNA

ABSTRACT: We performed transcriptome analysis of HCAECs upon treatment with siRNF213 or with a control siRNA. Overall, a total of 217 genes were up-regulated (> 2.0-fold change in expression), while 499 genes were down-regulated (< 0.5-fold change in expression), in the siRNF213-treated cells when compared to the control. Expression of four genes (RNF213, CyclinA, B and E) from this signature was quantified in the same RNA samples by real-time PCR.

ORGANISM(S): Homo sapiens

PROVIDER: GSE62348 | GEO | 2015/08/10

SECONDARY ACCESSION(S): PRJNA263898

REPOSITORIES: GEO

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Gene expression profile in HCAECs transfected with RNF213 siRNA

Project description:We performed transcriptome analysis of HCAECs upon treatment with siRNF213 or with a control siRNA. Overall, a total of 217 genes were up-regulated (> 2.0-fold change in expression), while 499 genes were down-regulated (< 0.5-fold change in expression), in the siRNF213-treated cells when compared to the control. Expression of four genes (RNF213, CyclinA, B and E) from this signature was quantified in the same RNA samples by real-time PCR. Gene expression in HCAECs upon treatment with siRNF213 or with a control siRNA. Two independent experiments were performed at each condition.

2015-08-10 | E-GEOD-62348 | biostudies-arrayexpress

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RNF213-associated urticarial lesions with hypercytokinemia

Project description:Urticarial lesions are observed in both cutaneous and systemic disorders. Familial forms of urticarial syndromes are rare and can be encountered in systemic auto-inflammatory diseases. We investigated a large family with dominantly inherited chronic urticarial lesions associated with hypercytokinemia. We performed a genetic linkage analysis in 14 patients from a 5-generation family, as well as whole-exome sequencing, cytokine profiling and transcriptomic analyses on samples from two patients. The identified candidate protein was studied after in vitro expression of the corresponding normal and mutated recombinant proteins. An unsupervised proteomic approach was followed to unveil the associated protein network. The disease phenotype of the most affected family members is characterized by chronic urticarial flares associated with extremely high plasma levels of pro- (IL-1b, IL-6, TNF-a) and anti-inflammatory (IL-10, IL1-RA) cytokines, with no secondary organ dysfunction, no susceptibility to infections, no fever and normal C-reactive protein levels. Monocyte transcriptomic analyses identified an immunotolerant profile in the most affected patient. Affected family members carried a loss-of-function mutation in RNF213 that encodes mysterin, a protein of poorly known physiological role. We identified the deubiquitinase CYLD, a major regulator of inflammation, as an RNF213 partner and showed that CYLD expression is inhibited by wild-type but not mutant RNF213. We identified a new entity characterized by chronic urticarial lesions associated with a clinically-blunted hypercytokinemia. This disease, due to a loss of function of RNF213, reveals mysterin’s key role in the complex molecular network of innate immunity.

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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

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Project description:To map the genome-wide DNA binding sites of the transcription factor PRDM15 in HCAECs, we generated PRDM15-overexpressing (PRDM15-OE) HCAECs and corresponding empty vector-infected controls. CUT&Tag assays were performed in biological triplicate for both PRDM15-OE and control groups.

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Project description:RNF213 is a large, poorly characterized interferon-induced protein. Mutations in RNF213 are associated with predisposition for Moyamoya disease (MMD), a rare cerebrovascular disorder. Recently, RNF213 was found to have broad antimicrobial activity in vitro and in vivo, yet the molecular mechanisms behind this function remain unclear. Using mass spectrometry-based proteomics and validation by real-time PCR we here report that knockdown of RNF213 leads to transcriptional upregulation of MVP and downregulation of CYR61, in line with reported pro- and anti-bacterial activities of these proteins. Knockdown of RNF213 also results in downregulation of DDAH1, which we discover to exert anti-microbial activity against Listeria monocytogenes infection. DDAH1 regulates production nitric oxide (NO), a molecule with both vascular and antimicrobial effects. We show that NO production is reduced in macrophages from RNF213 KO mice, suggesting that RNF213 controls Listeria infection through regulation of DDAH1 transcription and production of NO. Our findings propose a potential mechanism for the antilisterial activity of RNF213 and highlight NO as a potential link between RNF213-mediated immune responses and the development of MMD.

2022-02-17 | PXD027130 | Pride

RNF213-associated urticarial lesions with hypercytokinemia

Project description:RNF213-associated urticarial lesions with hypercytokinemia

| PRJNA713772 | ENA

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2014-02-20 | E-GEOD-44596 | biostudies-arrayexpress

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