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NRF2 is a key regulator of endothelial miRNA expression under pro-atherogenic stimuli

ABSTRACT: NRF2 is a key regulator of endothelial miRNA expression under pro-atherogenic stimuli

PROVIDER: PRJNA563721 | ENA |

REPOSITORIES: ENA

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NRF2 is a key regulator of endothelial miRNA expression under pro-atherogenic stimuli

Project description:Regulation of coding and non-coding genes is studied from primary human aortic endothelial cells (HAECs), venous endothelial cells (HUVECs), aortic smooth muscle cells (HASMCs) and macrophages (CD14+) under pro-atherogenic stimuli (hypoxia, oxPAPC and hypoxia+oxPAPC) by integrating three different sequencing techinques: GRO-seq, miRNA-seq and RNA-seq

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NRF2 is a key regulator of endothelial microRNA expression under proatherogenic stimuli.

Project description: Not available

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TNFalpha interferes with adaptation to starvation and activates pro-atherogenic processes

Project description:Pathenogenesis of atherosclerosis results from the interactions between disrupted lipid homeostasis and immune response, but the molecular bridges between the major players are still a matter of controversy. We performed a systemic study of the imflammatory cytokine tumor necrosis factor alpha (TNF alpha), a well established anorexia agent, in the livers of the mice exposed to 20h-cytokine/starvation. We show that treatment with TNF-alpha reverses adaptations to fasting. Moreover, it up-regulates cholesterol biosynthesis and down-regulates bile acids synthesis, which leads to disrupted cholesterol homeostasis and pro-atherogenic changes. Interestingly, we found that TNF alpha also interferes with gene regulation of the xenobiotic metabolism. Keywords: treatment and diet effects Mice have been either saline treated (nontreated group), saline treated and fasted for 20h (fasted group), and TNF-alpha treated (30 mikrograms per animal) and fasted for 20h (TNF-alpha group). 3 biological replicas from fasted and TNF-alpha groups were co-hybridized with pool of nontreated group. No dye-swaps were performed.

2010-05-25 | E-GEOD-6423 | biostudies-arrayexpress

Mitochondrial 3243A > G mutation confers pro-atherogenic and pro-inflammatory properties in MELAS iPS derived endothelial cells

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TNFalpha interferes with adaptation to starvation and activates pro-atherogenic processes

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Nrf2 transcript alterations

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Atherogenic Stimuli Trigger Ago2-hnRNP A1-Dependent Processing of RNYs Regulating Apoptosis and Inflammatory Response in Macrophages

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CCD18co colonic fibroblast cell line treated with various pro-inflammatory stimuli, and analized by single cell RNA sequencing (scRNA-seq) to analyze pro-fibrotic signatures

Project description:CCD18co cells are representative of colonic human fibroblasts. We wanted to understand if there was a stimulus that could induce the cells to acquire the same pro-fibrotic signatures that are found in patients with Ulcerative Colitis or Crohn's Disease. We stimulated the cells with various pro-fibrotic stimuli, and analyzed the signatures by single cell RNA sequencing (scRNA-seq)

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Transgenic expression of Nrf2 in the mouse

Project description:NFE2L2, nuclear factor, erythroid 2 like 2 (Nrf2), is a transcription factor that protects cells through maintaining a homeostatic redox state during stress. Constitutive expression of Nrf2 (CaNrf2-TG) was previously shown to be pathological to the heart over time. We tested a hypothesis that the cardiac-specific expression of full length Nrf2 (mNrf2-TG) would moderately increase the basal antioxidant defense, triggering a pro-reductive environment leading to adaptive cardiac remodeling.

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Functional analysis of the cytoprotective transcription factor Nrf2 in keratinocytes: Identification of Nrf2-regulated miRNAs

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