scholarly journals Localization of fibroblast growth factor-2 (basic FGF) and FGF receptor-1 in adult human kidney11See Editorial by Barasch, p. 1156.

1999 ◽  
Vol 56 (3) ◽  
pp. 883-897 ◽  
Author(s):  
Jürgen Floege ◽  
Kelly L. Hudkins ◽  
Frank Eitner ◽  
Yan Cui ◽  
Richard S. Morrison ◽  
...  
1996 ◽  
Vol 271 (10) ◽  
pp. 5663-5670 ◽  
Author(s):  
Agnes Estival ◽  
Veronique Monzat ◽  
Karine Miquel ◽  
François Gaubert ◽  
Etienne Hollande ◽  
...  

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.


1994 ◽  
Vol 142 (2) ◽  
pp. 325-338 ◽  
Author(s):  
G P Becks ◽  
A Logan ◽  
I D Phillips ◽  
J-F Wang ◽  
C Smith ◽  
...  

Abstract Goitre was induced in adult rats by acute (1 or 2 weeks) or chronic (4 or 10 weeks) administration of methimazole together with a low iodine diet. Involution of thyroid growth was then observed at 16 weeks, 4 weeks after withdrawal of goitrogens and reversion to a normal diet. Experimental animals quickly became hypothyroid compared with controls and exhibited thyroid hyperplasia (control (n=10): total serum thyroxine (T4) 66 ±4 nmol/l, thyroid weight 5 ± 1 mg/100 g body weight, means± s.d.; experimental (n=10): T4 undetectable, thyroid weight 27 ±4 mg/100 g body weight after 2 weeks of treatment). Thyroid growth rate subsequently slowed between 2 and 10 weeks. Messenger RNA for basic fibroblast growth factor (basic FGF) and for the high-affinity FGF receptor, was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for basic FGF and its receptor were detectable in thyroids from control rats at all times, while none was detected in the livers from any animal. Basic FGF and receptor mRNAs increased, and were detected at greatest abundance in hyperplastic thyroids at 1 and 2 weeks respectively, during goitre formation, but subsequently declined in parallel with thyroid growth rate at 4 and 10 weeks. When quantified by radioimmunoassay, basic FGF extracted from thyroids was fivefold greater than in controls after 1 week of goitrogen treatment (control (n=4): 24±9 pmol/μg DNA; goitre (n=4): 100± 16 pmol/μg DNA; P<0·05). Basic FGF and FGF receptor mRNAs localized by in situ hybridization predominantly to the epithelial cell population within follicles. Localization by immunohistochemistry demonstrated that basic FGF was present in the thyroids of control rats, and was largely associated with the basement membrane of follicles. During thyroid hyperplasia, increased basic FGF immunoreactivity appeared over the cytoplasm of follicular epithelial cells and was lost from the extracellular matrix. Thyroid involution following removal of goitrogen/low iodine treatment was associated with a decrease in mRNA for basic FGF or its receptor, and a loss of immunoreactive basic FGF from the cytoplasm of follicular cells. These results suggest that autocrine expression of basic FGF and FGF receptor could contribute to thyroid hyperplasia in rats. Journal of Endocrinology (1994) 142, 325–338


1990 ◽  
Vol 10 (9) ◽  
pp. 4728-4736
Author(s):  
D E Johnson ◽  
P L Lee ◽  
J Lu ◽  
L T Williams

We recently reported the isolation of a chicken cDNA clone encoding a basic fibroblast growth factor (FGF) receptor that has three immunoglobulinlike domains in the extracellular region. We have now identified four unique human cDNA clones encoding previously unknown FGF receptor variants which contain only two immunoglobulinlike domains. Two of the human clones encode membrane-spanning receptors, and two encode putative secreted forms. Both the three- and two-immunoglobulinlike-domain forms mediate biological responsiveness to acidic and basic FGF. Thus, the first immunoglobulinlike domain of the three-domain form may have a function other than binding of acidic and basic FGF.


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.


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