KREJČÍ, Pavel, B. MASRI, V. FONTAINE, P.B. MEKIKIAN, M. WEIS, H. PRATS and W.R. WILCOX. Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis. Journal of Cell Science. Cambridge: Company of Biologists Ltd., 2005, vol. 118, No 21, p. 5089-5100. ISSN 0021-9533. Available from: https://dx.doi.org/10.1242/jcs.02618.
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Basic information
Original name Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis.
Name in Czech Interaction of fibroblast growth factor and C-natriuretic peptide signaling inregulation of chondrocyte proliferation and extracellular matrix homeostasis.
Authors KREJČÍ, Pavel (203 Czech Republic, guarantor, belonging to the institution), B. MASRI (840 United States of America), V. FONTAINE (840 United States of America), P.B. MEKIKIAN (840 United States of America), M. WEIS (840 United States of America), H. PRATS (840 United States of America) and W.R. WILCOX (840 United States of America).
Edition Journal of Cell Science, Cambridge, Company of Biologists Ltd. 2005, 0021-9533.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30105 Physiology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 6.543
RIV identification code RIV/00216224:14310/05:00059335
Organization unit Faculty of Science
Doi http://dx.doi.org/10.1242/jcs.02618
UT WoS 000233678700019
Keywords in English CYCLIC-GMP; ENDOCHONDRAL OSSIFICATION;INTERGLOBULAR DOMAIN; CARTILAGE AGGRECAN; PROTEIN-KINASES;
Changed by Changed by: Mgr. Jiřina Medalová, Ph.D., učo 176525. Changed: 20/3/2012 14:23.
Abstract
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 of rat 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. In addition, CNP compensated for FGF2-mediated matrix loss by upregulation of matrix production independent of its interference with FGF signaling. We conclude that CNP utilizes both direct and indirect ways to counteract the effects of FGF signaling in a chondrocyte environment.
Links
MSM0021622415, plan (intention)Name: Molekulární podstata buněčných a tkáňových regulací
Investor: Ministry of Education, Youth and Sports of the CR, Molecular basis of cell and tissue regulations
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