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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.

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

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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