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A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis [RNA-Seq]

ABSTRACT: We exploited a three-dimensional model of sprouting angiogenesis in which the phenotypic switch from quiescent ECs to tip cells was triggered by VEGF-A. The information obtained about modulated miRNAs and their related protein-coding gene targets was used to generate a co-expression network encompassing gene modules that are post-transcriptionally regulated and whose activity is required for sprouting.

ORGANISM(S): Homo sapiens

PROVIDER: GSE115817 | GEO | 2020/01/21

REPOSITORIES: GEO

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A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis [shDICER]

Project description:We exploited a three-dimensional model of sprouting angiogenesis in which the phenotypic switch from quiescent ECs to tip cells was triggered by VEGF-A. The information obtained about modulated miRNAs and their related protein-coding gene targets was used to generate a co-expression network encompassing gene modules that are post-transcriptionally regulated and whose activity is required for sprouting.

2020-01-21 | GSE116039 | GEO

A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis [2D]

2020-01-21 | GSE129275 | GEO

A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis [miRNA-seq]

2020-01-21 | GSE115954 | GEO

The histone acetyltransferase HBO1 (KAT7) promotes efficient tip cell sprouting during angiogenesis

Project description:Blood vessel growth and remodelling are essential during embryonic development and disease pathogenesis. The diversity of endothelial cells (ECs) is transcriptionally evident and ECs undergo dynamic changes in gene expression during vessel growth and remodelling.Here, we investigated the role of the histone acetyltransferase HBO1 (KAT7), which is important for activating genes during development and histone H3 lysine 14 acetylation (H3K14ac). Loss of HBO1 and H3K14ac impaired developmental sprouting angiogenesis and reduced pathological EC overgrowth in the retinal endothelium. Single-cell RNA-sequencing of retinal ECs revealed an increased abundance of tip cells in Hbo1 deleted retinas, which lead to EC overcrowding in the retinal sprouting front and prevented efficient tip cell migration. We found that H3K14ac was highly abundant in the endothelial genome in both intra- and intergenic regions suggesting that the role of HBO1 is as a genome organiser that promotes efficient tip cell behaviour necessary for sprouting angiogenesis.

2021-09-30 | GSE161310 | GEO

The histone acetyltransferase HBO1 (KAT7) promotes efficient tip cell sprouting during angiogenesis

2021-09-30 | GSE161236 | GEO

Loss of apelin blocks the emergence of sprouting angiogenesis in experimental tumors

Project description:Angiogenesis-inhibitor (AI) drugs targeting vascular endothelial growth factor (VEGF) signalling to the endothelial cell (EC) are used to treat various cancers types. However, primary or secondary resistance to therapy is common. Clinical and pre-clinical studies suggest that other alternative pro-angiogenic factors are up-regulated after VEGF-pathway inhibition. Therefore, identification alternative pro-angiogenic pathway(s) is critical for the development of more effective anti-angiogenic therapy. Here we study the role of apelin as a pro-angiogenic G-protein coupled receptor (GPCR) ligand in tumor growth and angiogenesis. We applied single-cell RNA-sequencing to Mouse Lewis lung carcinoma (LLC1) or B16F10 mouse melanoma cell lines (1 X 106) implanted subcutaneously into the flanks of 12 weeks old Apln-/y or littermate control mice in combination with sunitinib or control (vehicle) treatment. We found apelin loss reduced angiogenic sprouting and tip cell marker gene expression in comparison to the sunitinib-alone treated mice and prevented EC tip cell differentiation.

2023-04-06 | E-MTAB-11663 | biostudies-arrayexpress

Endothelial TDP-43 controls sprouting angiogenesis and vascular barrier integrity, and its deletion triggers neuroinflammation

Project description:TDP-43 is a DNA/RNA-binding protein that regulates gene expression and its malfunction in neurons has been causally associated with multiple neurodegenerative disorders. Although progress has been made in understanding the functions of TDP-43 in neurons, little is known about its role in endothelial cells (ECs), angiogenesis and vascular function. Using inducible EC-specific TDP-43 knockout mice, we show that TDP-43 is required for sprouting angiogenesis, vascular barrier integrity and blood vessel stability. Postnatal EC-specific deletion of TDP-43 leads to retinal hypovascularization due to defects in vessel sprouting associated with reduced EC proliferation and migration. In mature blood vessels, loss of TDP-43 disrupts the blood-brain barrier and triggers vascular degeneration. These vascular defects are associated with an inflammatory response in the central-nervous system with activation of microglia and astrocytes. Mechanistically, deletion of TDP-43 disrupts fibronectin matrix around sprouting vessels and reduces -catenin signaling in ECs. Together, our results indicate that TDP-43 is essential for the formation of a stable and mature vasculature.

2024-02-01 | GSE253868 | GEO

Cx40 Suppresses Sprouting Angiogenesis In Vitro

Project description:Blood vessels are highly organized and form during development through a series of complex processes that include vasculogenesis, sprouting angiogenesis, and vessel remodeling. Several gap junction proteins (termed connexins, Cx) – including Cx40 (GJA5) – are expressed in vascular endothelium early during vessel development and are critical for establishment of a healthy vasculature. However, Cx40’s specific role in regulating vessel growth remains uncertain: while previous studies have shown that developmental and cancer-associated neovascularization is reduced in Cx40-knockout mice, Cx40 knockout in zebrafish embryos enhances intersegmental vessel growth. Thus, in the current study, our aim was to identify Cx40’s specific role in sprouting angiogenesis. First, we used a vessel-on-a-chip microphysiological model to confirm Cx40’s overall necessity for microvessel network development. Next, we used the fibrin gel bead assay – a three-dimensional in vitro model of sprouting angiogenesis – to assess Cx40’s necessity for this process. We found that Cx40 knockdown in endothelial cells drives more aggressive sprouting angiogenesis in association with increased endothelial cell proliferation. By contrast, using Electrical Cell-substrate Impedance Sensing (ECIS) we observed no effect of Cx40 knockdown on endothelial cell migration. Lastly, we found that Cx37 (GJA4) is reduced in Cx40- deficient endothelial cells, and that targeted silencing of Cx37 alone produces a more aggressive, hyper-sprouting phenotype compared to control or Cx40 knockdown endothelial cells. Taken together, our data argue that Cx40 plays multiple roles during vessel growth, including to specifically limit sprouting angiogenesis, and that this may occur (at least in part) through regulation of endothelial Cx37 levels.

2023-12-14 | GSE243404 | GEO

A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis

Project description:A Regulatory microRNA Network Controls Endothelial Cell Phenotypic Switch During Sprouting Angiogenesis

| PRJNA530705 | ENA

Single-cell transcriptome of wet AMD patient-derived endothelial cells in angiogenic sprouting

Project description:Age-related macular degeneration (AMD) is a global leading cause of visual impairment in older populations. ‘Wet’ AMD, the most common subtype of this disease, occurs when pathological angiogenesis infiltrates the subretinal space (choroidal neovascularization), causing hemorrhage and retinal damage. Gold standard anti-vascular endothelial growth factor (VEGF) treatment is an effective therapy, but the long-term prevention of visual decline has not been as successful. This warrants the need to elucidate potential VEGF-independent pathways. We generated blood out-growth endothelial cells (BOECs) from wet AMD and normal control subjects, then induced angiogenic sprouting of BOECs using a fibrin gel bead assay. To deconvolute endothelial heterogeneity, we performed single-cell transcriptomic analysis on the sprouting BOECs, revealing a spectrum of cell states. Our wet AMD BOECs share common pathways with choroidal neovascularization such as extracellular matrix remodeling that promoted proangiogenic phenotype, and our ‘activated’ BOEC subpopulation demonstrated proinflammatory hallmarks, resembling the tip-like cells in vivo. We uncovered new molecular insights that pathological angiogenesis in wet AMD BOECs could also be driven by interleukin signaling and amino acid metabolism. A web-based visualization of the sprouting BOEC single-cell transcriptome (https://christinecheunglab.shinyapps.io/human_wet_AMD_sprouting/) has been created to facilitate further discovery research.

2022-11-02 | GSE213933 | GEO

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