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Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [RNA-seq]

ABSTRACT: Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [RNA-seq]

PROVIDER: PRJNA488080 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7759380.fastq.gz	Fastqsanger.gz
	SRR7759381.fastq.gz	Fastqsanger.gz
	SRR7759382.fastq.gz	Fastqsanger.gz
	SRR7759379.fastq.gz	Fastqsanger.gz

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Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [RNA-seq]

Project description:Vascular inflammation is present in many cardiovascular diseases and exogenous glucocorticoids have traditionally been used as a therapy to suppress inflammation. However, recent data has shown that endogenous glucocorticoids, acting through the endothelial glucocorticoid receptor, act as negative regulators of inflammation. Here we performed chromatin immunoprecipitation for the glucocorticoid receptor followed by next-gen sequencing in mouse endothelial cells to investigate how the endothelial glucocorticoid receptor regulates vascular inflammation. We identified a novel role of the Wnt signaling pathway in this setting and show that loss of the endothelial glucocorticoid receptor results in up regulation of Wnt signaling both in vitro and in vivo using our validated mouse model. Further we demonstrate glucocorticoid receptor regulation of a key gene in the Wnt pathway via a novel glucocorticoid response element gleaned from our genomic data. These results suggest a novel role for endothelial Wnt signaling modulation in states of vascular inflammation.

2020-04-07 | GSE119092 | GEO

Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [ChIP-seq]

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Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway

Project description:Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway

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Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [ChIP-seq]

Project description:Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway [ChIP-seq]

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Genomic landscape of endothelial cell-glucocorticoid receptor interactions: Regulation of the Wnt signaling pathway

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-04-07 | GSE119093 | GEO

Endothelial cell-glucocorticoid receptor interactions and regulation of Wnt signaling.

Project description:Vascular inflammation is present in many cardiovascular diseases, and exogenous glucocorticoids have traditionally been used as a therapy to suppress inflammation. However, recent data have shown that endogenous glucocorticoids, acting through the endothelial glucocorticoid receptor, act as negative regulators of inflammation. Here, we performed ChIP for the glucocorticoid receptor, followed by next-generation sequencing in mouse endothelial cells to investigate how the endothelial glucocorticoid receptor regulates vascular inflammation. We identified a role of the Wnt signaling pathway in this setting and show that loss of the endothelial glucocorticoid receptor results in upregulation of Wnt signaling both in vitro and in vivo using our validated mouse model. Furthermore, we demonstrate glucocorticoid receptor regulation of a key gene in the Wnt pathway, Frzb, via a glucocorticoid response element gleaned from our genomic data. These results suggest a role for endothelial Wnt signaling modulation in states of vascular inflammation.

| S-EPMC7098785 | biostudies-literature

Osteoblast-Endothelial Transition Contributes to Glucocorticoid-Induced Bone Loss

Project description:To investigate the transition of osteoblast to endothelial-like cell in glucocorticoid induced osteoporosis. We performed gene expression profiling analysis using data obtained from RNA-seq of dexamethasone treated vs control.

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Interactions between genistein and Wnt pathway in colon adenocarcinoma and early embryos

Project description:Interactions between genistein and Wnt pathway in colon adenocarcinoma and early embryos

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Osteoblast-Endothelial Transition Contributes to Glucocorticoid-Induced Bone Loss

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Loss of endothelial glucocorticoid receptor promotes angiogenesis via upregulation of Wnt/β-catenin pathway.

Project description:ObjectiveThe glucocorticoid receptor (GR) is a member of the nuclear receptor family that controls key biological processes in the cardiovascular system and has recently been shown to modulate Wnt signaling in endothelial cells. Wnt/β-catenin signaling has been demonstrated to be crucial in the process of angiogenesis. In the current study, we studied whether GR could regulate angiogenesis via the Wnt/β-catenin pathway.Approach and resultsaKey components of the Wnt/β-catenin pathway were evaluated using quantitative PCR and Western blot in the presence or absence of GR. Enhanced angiogenesis was found in GR deficiency in vitro and confirmed with cell viability assays, proliferation assays and tube formation assays. Consistent with these in vitro findings, endothelial cell-specific GR loss GR in vivo promoted angiogenesis in both a hind limb ischemia model and sponge implantation assay. Results were further verified in a novel mouse model lacking endothelial LRP5/6, a key receptor in canonical Wnt signaling, and showed substantially suppressed angiogenesis using these same in vitro and in vivo assays. To further investigate the mechanism of GR regulation of Wnt signaling, autophagy flux was investigated in endothelial cells by visualizing auto phagolysosomes as well as by assessing P62 degradation and LC3B conversion. Results indicated that potentiated autophagy flux participated in GR-Wnt regulation.ConclusionsLack of endothelial GR triggers autophagy flux, leads to activation of Wnt/β-catenin signaling and promotes angiogenesis. There may also be a synergistic interaction between autophagy and Wnt/β-catenin signaling.

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