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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.

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

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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