Effective myofibroblast dedifferentiation by concomitant inhibition of TGF-beta signaling and perturbation of MAPK signaling

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F13%3A00435856" target="_blank" >RIV/68378050:_____/13:00435856 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.ejcb.2013.10.013" target="_blank" >http://dx.doi.org/10.1016/j.ejcb.2013.10.013</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.ejcb.2013.10.013" target="_blank" >10.1016/j.ejcb.2013.10.013</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Effective myofibroblast dedifferentiation by concomitant inhibition of TGF-beta signaling and perturbation of MAPK signaling

Popis výsledku v původním jazyce

Fibrotic diseases are a group of pathologies with high incidence and mortality. Despite extensive research efforts, effective therapies are still not available. Understanding the molecular mechanisms driving the onset, progression and possible resolutionof fibrosis is a prerequisite to the development of successful therapies. The central role of the TGF-beta pathway and myofibroblasts in the pathogenesis of fibrosis is now generally accepted. The possible mechanisms of myofibroblast elimination or dedifferentiation, on the other hand, are still almost uncharted territory. Here we show that sustained expression of some components of MAPK signaling pathway (PDGFB, Ha-Ras(G12V) or the transcription factor EGR4) in primary chicken embryo dermal myofibroblasts results in a loss of autocrine TGF-beta signaling and suppression of the myofibroblastic phenotype, characterized by the loss of alpha smooth muscle actin fibers and a substantial reduction in the production of extracellular matrix.

Název v anglickém jazyce

Effective myofibroblast dedifferentiation by concomitant inhibition of TGF-beta signaling and perturbation of MAPK signaling

Popis výsledku anglicky

Fibrotic diseases are a group of pathologies with high incidence and mortality. Despite extensive research efforts, effective therapies are still not available. Understanding the molecular mechanisms driving the onset, progression and possible resolutionof fibrosis is a prerequisite to the development of successful therapies. The central role of the TGF-beta pathway and myofibroblasts in the pathogenesis of fibrosis is now generally accepted. The possible mechanisms of myofibroblast elimination or dedifferentiation, on the other hand, are still almost uncharted territory. Here we show that sustained expression of some components of MAPK signaling pathway (PDGFB, Ha-Ras(G12V) or the transcription factor EGR4) in primary chicken embryo dermal myofibroblasts results in a loss of autocrine TGF-beta signaling and suppression of the myofibroblastic phenotype, characterized by the loss of alpha smooth muscle actin fibers and a substantial reduction in the production of extracellular matrix.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/KAN200520801" target="_blank" >KAN200520801: Cílená exprese a transport bioaktivních molekul</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

European Journal of Cell Biology

ISSN

0171-9335

e-ISSN

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Svazek periodika

92

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

11

Strana od-do

363-373

Kód UT WoS článku

000332133500002

EID výsledku v databázi Scopus

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