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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.

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

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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