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Endothelial RNA Modifications in Vascular Homeostasis and Disease

Total Cost €


EC-Contrib. €






 MODVASC project word cloud

Explore the words cloud of the MODVASC project. It provides you a very rough idea of what is the project "MODVASC" about.

discovery    atherosclerosis    adenosine    posttranscriptional    modification    critical    cover    multiprotein    phenotype    describe    stimuli    pivotal    disease    modvasc    induce    molecular    position    base    functional    play    cell    modifications    mortality    homeostasis    clinical    western    prevalent    mechanisms    orchestrate    protein    strategies    inflammatory    interactions    regulate    nucleotide    transcriptome    venous    biochemical    unknown    completely    critically    eukaryotic    explore    functions    consolidate    biomarkers    basal    140    risk    methylated    sequencing    nucleotides    unpublished    m6a    activation    immunoprecipitation    single    rna    preliminary    contribution    n6    accumulating    vascular    regulator    environmental    arterial    cells    alphabet    metabolism    tree    catalyzed    suggests    function    pro    methylation    biology    canonical    entire    methyltransferase    organ    cardiovascular    vivo    therapeutic    fate    followed    mrna    stress    relevance    endothelial    patients    world   

Project "MODVASC" data sheet

The following table provides information about the project.


Organization address
address: KINGS GATE
postcode: NE1 7RU

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 1˙499˙250 €
 EC max contribution 1˙499˙250 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-STG
 Funding Scheme ERC-STG
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2023-05-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 


 Project objective

Endothelial cells cover the entire arterial and venous tree, and play a pivotal role in vascular and organ homeostasis. In general, cardiovascular risk factors induce endothelial cell activation towards a pro-inflammatory phenotype leading to atherosclerosis, a major cause of mortality in the Western world. Understanding the mechanisms that orchestrate endothelial cell functions and response to environmental stimuli is essential for the discovery and development of novel biomarkers and therapeutic strategies in vascular disease. RNA base modifications increase the RNA alphabet from the 4 canonical nucleotides to more than 140. Adenosine methylation at the N6 position (m6A) is the most prevalent RNA modification in eukaryotic mRNA and is catalyzed by a multiprotein methyltransferase complex. Accumulating recent evidence suggests that m6A RNA methylation is a critical posttranscriptional regulator of RNA metabolism. In preliminary unpublished work we have identified methylated RNA targets, which may critically regulate endothelial cell functions. Since the impact of m6A RNA methylation on vascular function is completely unknown, MODVASC aims to explore the role of m6A RNA methylation in vascular growth, homeostasis and disease. By m6A-RNA immunoprecipitation followed by RNA-sequencing we will identify the transcriptome-wide m6A RNA methylation in endothelial cells under basal and stress conditions. With the help of advanced molecular biology and biochemical methods, we will describe in single nucleotide level the impact of m6A RNA methylation on mRNA fate and RNA-protein interactions and define its functional consequences in endothelial cell functions. In vivo studies will consolidate the impact of endothelial RNA methylation on vascular growth and homeostasis as well as its contribution to atherosclerosis. Finally, MODVASC will evaluate the clinical relevance of our findings in patients with cardiovascular disease.

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The information about "MODVASC" are provided by the European Opendata Portal: CORDIS opendata.

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