Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis.

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F05%3A00059335" target="_blank" >RIV/00216224:14310/05:00059335 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1242/jcs.02618" target="_blank" >http://dx.doi.org/10.1242/jcs.02618</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1242/jcs.02618" target="_blank" >10.1242/jcs.02618</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis.

Popis výsledku v původním jazyce

Overexpression of C-natriuretic peptide (CNP) in cartilage partially rescues achondroplasia in the mouse. Here, we studied the interaction of fibroblast growth factor (FGF) and CNP signaling in chondrocytes. CNP antagonized FGF2-induced growth arrest ofrat chondrosarcoma (RCS) chondrocytes by inhibition of the Erk mitogen activated protein kinase pathway. This effect of CNP was protein kinase G-dependent and was mimicked by the cGMP analog pCPT-cGMP. FGF2-mediated activation of both MEK and Raf-1 but not Ras or FRS2 was abolished by CNP demonstrating that CNP blocks the Erk pathway at the level of Raf-1. CNP also counteracted the FGF2-mediated degradation of RCS extracellular matrix. CNP partially antagonized FGF2-induced expression, release and activation of several matrix-remodeling molecules including matrix metalloproteinase 2 (MMP2), MMP3, MMP9, MMP10 and MMP13.

Název v anglickém jazyce

Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis.

Popis výsledku anglicky

Overexpression of C-natriuretic peptide (CNP) in cartilage partially rescues achondroplasia in the mouse. Here, we studied the interaction of fibroblast growth factor (FGF) and CNP signaling in chondrocytes. CNP antagonized FGF2-induced growth arrest ofrat chondrosarcoma (RCS) chondrocytes by inhibition of the Erk mitogen activated protein kinase pathway. This effect of CNP was protein kinase G-dependent and was mimicked by the cGMP analog pCPT-cGMP. FGF2-mediated activation of both MEK and Raf-1 but not Ras or FRS2 was abolished by CNP demonstrating that CNP blocks the Erk pathway at the level of Raf-1. CNP also counteracted the FGF2-mediated degradation of RCS extracellular matrix. CNP partially antagonized FGF2-induced expression, release and activation of several matrix-remodeling molecules including matrix metalloproteinase 2 (MMP2), MMP3, MMP9, MMP10 and MMP13.

Druh

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

CEP obor

ED - Fyziologie

OECD FORD obor

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Projekt

—

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2005

Kód důvěrnosti údajů

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

Název periodika

Journal of Cell Science

ISSN

0021-9533

e-ISSN

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Svazek periodika

118

Číslo periodika v rámci svazku

21

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

12

Strana od-do

5089-5100

Kód UT WoS článku

000233678700019

EID výsledku v databázi Scopus

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