A complex role for FGF-2 in self renewal, survival, and adhesion of human embryonic stem cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F09%3A00028586" target="_blank" >RIV/00216224:14110/09:00028586 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/09:5364 RIV/68378041:_____/09:00332572

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

A complex role for FGF-2 in self renewal, survival, and adhesion of human embryonic stem cells

Popis výsledku v původním jazyce

The transcription program that is responsible for the pluripotency of human ESCs (hESCs) is believed to be comaintained by exogenous fibroblast growth factor-2 (FGF-2), which activates FGF receptors (FGFRs) and stimulates the mitogen-activated protein kinase (MAPK) pathway. This mechanism is further complicated by intracrine FGF signals.Here we show that, in undifferentiated hESCs, exogenous FGF-2 and inhibition of autocrine FGF signaling stimulated the expression of stem cell genes while suppressing cell death and apoptosis genes. Thus, exogenous FGF-2 reinforced the pluripotency maintenance program of intracrine FGF-2 signaling. Consistent with this hypothesis, expression of endogenous FGF-2 decreased during hESC differentiation and FGF-2 knockdown-induced hESC differentiation. In addition, FGF-2 signaling via FGFR2 activated MAPK kinase/extracellular signal-regulated kinase and AKT kinases, protected hESC from stress-induced cell death, and increased hESC adhesion and cloning effici

Název v anglickém jazyce

A complex role for FGF-2 in self renewal, survival, and adhesion of human embryonic stem cells

Popis výsledku anglicky

The transcription program that is responsible for the pluripotency of human ESCs (hESCs) is believed to be comaintained by exogenous fibroblast growth factor-2 (FGF-2), which activates FGF receptors (FGFRs) and stimulates the mitogen-activated protein kinase (MAPK) pathway. This mechanism is further complicated by intracrine FGF signals.Here we show that, in undifferentiated hESCs, exogenous FGF-2 and inhibition of autocrine FGF signaling stimulated the expression of stem cell genes while suppressing cell death and apoptosis genes. Thus, exogenous FGF-2 reinforced the pluripotency maintenance program of intracrine FGF-2 signaling. Consistent with this hypothesis, expression of endogenous FGF-2 decreased during hESC differentiation and FGF-2 knockdown-induced hESC differentiation. In addition, FGF-2 signaling via FGFR2 activated MAPK kinase/extracellular signal-regulated kinase and AKT kinases, protected hESC from stress-induced cell death, and increased hESC adhesion and cloning effici

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

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)<br>S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2009

Kód důvěrnosti údajů

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

Název periodika

Stem Cells

ISSN

1066-5099

e-ISSN

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Svazek periodika

2009

Číslo periodika v rámci svazku

27

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

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Kód UT WoS článku

000270050900016

EID výsledku v databázi Scopus

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