scholarly journals Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination

Author(s):  
Donna J. Messersmith ◽  
Joshua C. Murtie ◽  
Tuan Q. Le ◽  
Emma E. Frost ◽  
Regina C. Armstrong
1999 ◽  
Vol 77 (6) ◽  
pp. 569-575 ◽  
Author(s):  
Paramjit S Tappia ◽  
Raymond R Padua ◽  
Vincenzo Panagia ◽  
Elissavet Kardami

Although fibroblast growth factor-2 (FGF-2) plays an important role in cardioprotection and growth, little is known about the signals triggered by it in the adult heart. We therefore examined FGF-2-induced effects on phosphoinositide-specific phospholipase C (PI-PLC) isozymes, which produce second messengers linked to the inotropic and hypertrophic response of the myocardium. FGF-2, administered by retrograde perfusion to the isolated heart, induced an increase in inositol-1,4,5-trisphosphate levels in the cytosol, as well as an increase in total PI-PLC activity associated with sarcolemmal and cytosolic fractions. Furthermore FGF-2 induced a time-dependent elevation in cardiomyocyte membrane-associated PLC gamma1 and PLC β1 activities, assayed in immunoprecipitated fractions, and moreover, increased the membrane levels of PLC β1 and PLC β3. Activation of PLC β is suggestive of FGF-2-induced cross-talk between FGF-receptor tyrosine kinase and G-protein-coupled signaling in adult cardiomyocytes and underscores the importance of FGF-2 in cardiac physiology.Key words: FGF-2, signal transduction, PLC gamma, PLC β, cardiomyocytes.


1999 ◽  
Vol 56 (3) ◽  
pp. 883-897 ◽  
Author(s):  
Jürgen Floege ◽  
Kelly L. Hudkins ◽  
Frank Eitner ◽  
Yan Cui ◽  
Richard S. Morrison ◽  
...  

1994 ◽  
Vol 5 (8) ◽  
pp. 851-862 ◽  
Author(s):  
P Savagner ◽  
A M Vallés ◽  
J Jouanneau ◽  
K M Yamada ◽  
J P Thiery

We described previously that acidic fibroblast growth factor (aFGF), but not basic fibroblast growth factor (bFGF), can induce the rat carcinoma cell line NBT-II to undergo a rapid and reversible transition from epithelial to mesenchymal phenotype (EMT). We now find that NBT-II EMT is stimulated by keratinocyte growth factor (KGF) in cells grown at low density. Accordingly, a high-affinity receptor showing 98% homology to mouse FGF receptor 2b/KGF receptor was cloned and sequenced from NBT-II cells. Northern analysis indicated that mRNA for FGF receptor 2b/KGF receptor was drastically down-regulated within 1 wk in aFGF-induced mesenchymal NBT-II cells. This decrease coincided with an up-regulation of FGF receptor 2c/Bek, a KGF-insensitive, alternatively spliced form of FGF receptor 2b/KGF receptor. Functional studies confirmed that KGF could not maintain EMT induction on mesenchymal NBT-II cells. FGF receptor 1 and FGF receptor 2c/Bek could also support EMT induction when transfected into NBT-II cells in response to aFGF or bFGF. Such transfected cells could bind bFGF as well as aFGF. Therefore, EMT can be induced through different FGF receptors, but EMT may also regulate FGF receptor expression itself.


2001 ◽  
Vol 12 (2) ◽  
pp. 449-462 ◽  
Author(s):  
Hu Peng ◽  
John Moffett ◽  
Jason Myers ◽  
Xiaohong Fang ◽  
Ewa K. Stachowiak ◽  
...  

In bovine adrenal medullary cells synergistically acting type 1 and type 2 angiotensin II (AII) receptors activate the fibroblast growth factor-2 (FGF-2) gene through a unique AII-responsive promoter element. Both the type 1 and type 2 AII receptors and the downstream cyclic adenosine 1′,3′-monophosphate- and protein kinase C-dependent signaling pathways activate the FGF-2 promoter through a novel signal-transducing mechanism. This mechanism, which we have named integrative nuclear FGF receptor-1 signaling, involves the nuclear translocation of FGF receptor-1 and its subsequent transactivation of the AII-responsive element in the FGF-2 promoter.


Blood ◽  
1992 ◽  
Vol 80 (8) ◽  
pp. 1905-1913 ◽  
Author(s):  
A Bikfalvi ◽  
ZC Han ◽  
G Fuhrmann

Abstract We have investigated the interaction of fibroblast growth factor (FGF) with megakaryocytopoiesis. Acidic FGF (aFGF) stimulated the proliferation of murine megakaryocytes and human erythroleukemia (HEL) cells in a concentration-dependent manner. The concentrations of aFGF required to elicit half-maximum and maximum effects were similar for HEL and megakaryocytic colony formation. The effect of aFGF was comparable to that of basic FGF (bFGF) in both cell types. The effect of both FGFs was found to be synergistic with interleukin-3 (IL-3), and was abrogated by a monoclonal anti-IL-6 antibody. A specific cell surface receptor complex of approximately 120 Kd was detected for FGF by crosslinking experiments on HEL cells and total bone marrow (BM) cells. Single-cell autoradiography of megakaryocytes in BM smears and BM cultures showed binding sites for 125I-aFGF. Northern blot analysis of messenger RNA (mRNA) from total BM and HEL cells showed a 4.4-kb mRNA specific for FGF receptors type 1 (flg) and type 2 (bek). This was confirmed by polymerase chain reaction, which also showed the presence of FGF receptor mRNA in megakaryocytic-like cells, normal megakaryocytes, and platelets. Together, these results indicate that FGF is involved in megakaryocytopoiesis and suggest that this interaction may be mediated via FGF receptor type 1 and type 2 located on the megakaryocytic lineage or on accessory cells responsible for the release of megakaryocytic growth-promoting activities.


2008 ◽  
Vol 447 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Monica Frinchi ◽  
Alessandra Bonomo ◽  
Angela Trovato-Salinaro ◽  
Daniele F. Condorelli ◽  
Kjell Fuxe ◽  
...  

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