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Influence of Anti-VEGFA and dexamathasone treatments on the early phase of cornea angiogenesis

ABSTRACT: Inflammation is a key component of pathological angiogenesis. Here we monitor gene expression profiles of the pre-sprouting phase of corneal angiogenesis in the rat model, as influenced by topically applied treatments. We used GeneChip Rat Genome 230 2.0 Array to monitor gene expression profies of several genes in the different treatment groups

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE87330 | GEO | 2017/02/28

SECONDARY ACCESSION(S): PRJNA344417

REPOSITORIES: GEO

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Expression data from Rattus norvegicus cornea

Project description:Inflammation is a key component of pathological angiogenesis. Here we induce cornea neovascularisation using sutures placed into the cornea, and sutures are removed to induce a regression phase. We used whole transcriptome microarray to monitor gene expression profies of several genes

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Gene expression during first day of collagen gel culture of rat aortic rings

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Gene expression during first day of collagen gel culture of rat aortic rings

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Gene expression in TNF treated rat aortic rings cultured in collagen or fibrin gels.

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Gene expression in TNF treated rat aortic rings cultured in collagen or fibrin gels.

Project description:Angiogenesis in cultures of rat aorta begins with neovessels sprouting from the aortic explant within the first three days of culture. We used microarrys to examine the effects of TNF-alpha on gene expression in both fibrin and collagen gels during the first 48 hours or culture. Rat aortic rings were cultured in either collagen or fibrin maticies. Half of the cultures from each matrix group were treated with 10ng/ml recombinant rat TNF-alpha, and half were left untreated. These cultures were used to prepare total RNA

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Cx40 Suppresses Sprouting Angiogenesis In Vitro

Project description:Cx40 Suppresses Sprouting Angiogenesis In Vitro

| PRJNA1018433 | ENA

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.

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Genes associated with angiogenic response to Ang-1 or VEGF

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

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.

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