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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.

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

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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