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EXPLOSIA SIGNED

EXpansion and Phenotype Loss Of SMCs In Atherosclerosis: Causal effects and therapeutic possibilities

Total Cost €

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EC-Contrib. €

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Partnership

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 EXPLOSIA project word cloud

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

structure    questions    stabilises    single    modification    dichotomous    subtypes    hypothesis    lineage    arterial    entire    villains    architecture    muscle    human    manipulating    derives    forming    modulation    lipoproteins    density    accumulation    disease    deeper    hypothesise    completely    interventions    lose    clonal    functions    expansion    smooth    expression    recognition    smcs    wall    protective    drivers    cellular    founder    plaque    atherosclerosis    population    escaped    smc    macrophages    whereas    answer    uncovered    links    development    explosia    undergo    combining    causing    caused    lesion    prevent    carry    phenotype    strikingly    progression    humans    genes    tracking    rupture    transcriptomics    massive    balance    thrombosis    inflammatory    causal    function    activity    cell    immune    minipigs    fibrous    gene    modified    undergoing    atherosclerotic    signature    tissue    modulated    first    view    detection    conduct    phenotypic    central    programs    plaques    cells    perturbing    conventional    mice    techniques    few    dangerous    heroes    alter    found   

Project "EXPLOSIA" data sheet

The following table provides information about the project.

Coordinator
AARHUS UNIVERSITET 

Organization address
address: NORDRE RINGGADE 1
city: AARHUS C
postcode: 8000
website: www.au.dk

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 Denmark [DK]
 Total cost 1˙998˙875 €
 EC max contribution 1˙998˙875 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2025-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    AARHUS UNIVERSITET DK (AARHUS C) coordinator 1˙296˙120.00
2    CENTRO NACIONAL DE INVESTIGACIONESCARDIOVASCULARES CARLOS III (F.S.P.) ES (MADRID) participant 702˙755.00

Map

 Project objective

Atherosclerosis is considered an inflammatory disease caused by the accumulation, modification and immune cell recognition of low-density lipoproteins in the arterial wall. Plaque macrophages are held to be the main drivers of disease activity, whereas smooth muscle cells (SMCs) have traditionally been considered protective by forming fibrous tissue that stabilises plaques from undergoing rupture and causing thrombosis. In the present project, we challenge this dichotomous view of cellular villains and heroes in atherosclerosis. Using lineage tracking techniques in mice, we and others have uncovered a large population of SMCs in plaques, which has escaped detection because the cells completely lose conventional SMC phenotype. Strikingly, we have found that the entire plaque SMC population derives from only few founder SMCs that undergo massive clonal expansion and phenotypic modulation during lesion formation. We hypothesise that the balance between the different modulated SMC subtypes and the functions they carry are central to lesion progression. In EXPLOSIA we will address this hypothesis in 3 steps. First, we will conduct a comparative analysis of clonal structure in mice, minipigs, and humans. Second, we will determine links between SMC subtypes, their gene expression programs, and atherosclerotic disease activity by combining single-cell transcriptomics with novel techniques to alter atherosclerotic disease activity in gene-modified mice and minipigs. Third, we will develop techniques for manipulating genes in modulated plaque SMCs and test the causal role of perturbing SMC subtypes and function for lesion progression.

The aim of the project is to answer the following key questions for a deeper understanding of atherosclerosis: - What is the clonal architecture of SMCs in human atherosclerosis? - What is the SMC gene expression signature of atherosclerotic disease activity? - Can interventions targeting SMCs prevent dangerous lesion development?

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

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