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SEMA3C

Genetic dissection of the SEMA3C/Neuropilin 1 signalling pathway in Chronic Kidney Disease progression

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 SEMA3C project word cloud

Explore the words cloud of the SEMA3C project. It provides you a very rough idea of what is the project "SEMA3C" about.

worldwide    mechanisms    extracellular    sema3c    edge    paediatric    injury    cellular    proteins    mouse    incidence    engineered    initial    substantially    unravel    rearrangement    myofibroblast    genetically    epidemic    secreted    treatments    stages    functional    point    parenchyma    pathophysiology    deposition    directions    analysing    models    influence    play    kidney    population    cells    roles    morphology    insult    nrp1    events    function    diagnosis    deficient    chronic    producing    prealbuminuric    receptor    matrix    found    guidance    upregulated    biomarker    myofibroblasts    technologies    understand    interventions    characterised    organogenesis    semaphorins    pharmaceutical    ckd    regardless    proportions    mice    14    mechanistic    adult    disease    medical    destruction    ckds    signalling    planning    spectrum    proliferating    progression    levels    expressed    hallmark    surgically    nephrons    cutting    pathological    renal    fibrosis    reached    microvasculature    assay    progressive    glycoprotein    patients    human   

Project "SEMA3C" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

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 France [FR]
 Project website http://krctnn.com/
 Total cost 185˙076 €
 EC max contribution 185˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-09-05   to  2018-09-04

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 185˙076.00

Map

 Project objective

Regardless of the initial insult, human Chronic Kidney Disease (CKD) is characterised by progressive destruction of the renal parenchyma and the loss of functional nephrons. Renal fibrosis is the common end point of CKDs, the hallmark of which is the deposition of pathological matrix by myofibroblasts. The worldwide incidence of CKD has reached epidemic proportions with an estimated 10-14% of the adult population known to have CKD. A key challenge for medical planning is to better understand the mechanisms of CKD progression in order to target pharmaceutical interventions at the early stages of the disease. Semaphorins are guidance proteins which influence cellular morphology and function, and play important roles in organogenesis and disease. We found that the secreted glycoprotein SEMA3C was upregulated in two mouse models of kidney injury and in prealbuminuric stages of paediatric CKD patients. We also found that its receptor NRP1 was expressed in proliferating extracellular matrix-producing cells during CKD progression. We propose to use genetically engineered mice to investigate the function of the SEMA3C/NRP1 signalling pathway in CKD progression with three major objectives: 1. Investigate whether SEMA3C and its receptor NRP1 promote CKD progression by analysing the levels of surgically-induced renal injury in mice deficient for Sema3C and Nrp1. 2. Provide an improved mechanistic understanding of the disease by using cutting-edge technologies to unravel new signalling events promoting myofibroblast production and microvasculature rearrangement during kidney injury. 3. Assay the use of SEMA3C as a potential biomarker in the diagnosis of CKD and its progression. This work will substantially contribute to our current understanding of the pathophysiology of CKD and open up new directions for the development of novel treatments targeting this disease spectrum.

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The information about "SEMA3C" are provided by the European Opendata Portal: CORDIS opendata.

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