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REZONABLE

Regeneration and zonation by ZEB2 of Liver Endothelium

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 REZONABLE project word cloud

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

flows    waste    channels    proliferation    sinusoidal    found    transcription    metabolism    toxins    specified    lsec    blood    hypothesize    recovery    zonation    expressed    therapeutic    fenestrated    adult    removal    sip1    artery    proteins    contributes    hepatocytes    hereto    zeb2    cells    cultured    lined    relative    hepatocyte    injury    estimate    nutrient    sinusoids    chemotherapeutics    overexpression    endothelial    ecs    fibrosis    lsecs    central    overexpressing    specification    mice    transplantation    transcriptional    specialised    determinant    indispensible    transgenic    expression    maintenance    leaves    lab    position    organ    lacking    damage    portal    lentiviral    hepatic    parenchyma    agents    multidisciplinary    drugs    discontinuous    cirrhosis    receives    host    regeneration    time    veins    mix    liver    endothelium    body    dependent    progenitors    zones    pericentral    zone    disease    stimulate    mainly    oxygen    sinusoid    vein   

Project "REZONABLE" data sheet

The following table provides information about the project.

Coordinator
KATHOLIEKE UNIVERSITEIT LEUVEN 

Organization address
address: OUDE MARKT 13
city: LEUVEN
postcode: 3000
website: www.kuleuven.be

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 Belgium [BE]
 Total cost 160˙800 €
 EC max contribution 160˙800 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2016
 Duration (year-month-day) from 2016-01-01   to  2017-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KATHOLIEKE UNIVERSITEIT LEUVEN BE (LEUVEN) coordinator 160˙800.00

Map

 Project objective

The liver is a crucial organ in metabolism and removal of waste products from the body. Hereto, the liver parenchyma receives a mix of nutrient-rich blood from the portal vein and oxygen-rich blood from the hepatic artery. Blood flows through the sinusoids and leaves the liver via the central and hepatic veins. Hepatic sinusoids are highly specialised channels in which hepatocytes are organised in zones according to their position relative to the portal and central veins. They are lined with a specified, fenestrated, discontinuous endothelium. Many drugs (e.g., chemotherapeutics) and toxins cause damage to the sinusoids that may lead to liver fibrosis and cirrhosis. Formation of new sinusoids is an indispensible step for liver regeneration. Furthermore, liver sinusoidal endothelial cells (LSECs) produce agents that stimulate hepatocyte proliferation. Time-dependent expression of different proteins in the developing liver is important for sinusoid formation. The host lab found that the transcription factor Zeb2 (also known as Sip1) is highly expressed in LSECs in the developing and adult liver. Furthermore, its expression in adult LSECs is mainly in those from the pericentral zone. We hypothesize that Zeb2 is a transcriptional determinant of LSEC specification, zonation, maintenance and regeneration. Here, we aim to: (i) evaluate whether/how Zeb2 contributes to LSEC specification and zonation; (ii) establish a role for Zeb2 in LSECs in adult mice; (iii) assess its role in sinusoidal regeneration during liver disease; and (iv) estimate the therapeutic potential of Zeb2-treated endothelial progenitors in recovery from liver injury. To address these aims, we will use a multidisciplinary approach based on lentiviral overexpression in cultured ECs, transgenic mice lacking or overexpressing Zeb2 in ECs and transplantation of ECs pre-specified towards LSECs. These studies will allow us to evaluate the potential of Zeb2 as a novel target to stimulate liver regeneration.

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