scholarly journals Basic fibroblast growth factor in the chick embryo: immunolocalization to striated muscle cells and their precursors.

1989 ◽  
Vol 108 (6) ◽  
pp. 2459-2466 ◽  
Author(s):  
J Joseph-Silverstein ◽  
S A Consigli ◽  
K M Lyser ◽  
C Ver Pault
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Chick Embryo ◽  
Muscle Development ◽  
Striated Muscle ◽  
Muscle Cells ◽  
Limb Bud ◽  
Fibroblast Growth ◽  
Lack Of Information ◽  
Immunohistochemical Techniques

The identification of acidic and basic fibroblast growth factors (FGFs) in a number of embryonic tissue extracts has implicated these growth factors in the regulation of a variety of embryonic events including angiogenesis, eye development, and muscle differentiation. Lack of information concerning the cellular distribution of the growth factor within these tissues has made it extremely difficult to assign developmental roles to FGF. We have localized bFGF in the developing chick embryo using immunohistochemical techniques and our monospecific polyclonal rabbit anti-human bFGF IgG. The spatial pattern for bFGF localization was highly specific. The anti-human bFGF antibodies recognized striated muscle cells and their precursors in 2-6-d chick embryos. Myocardium, somite myotome, and limb bud muscle all stain positively for bFGF. In addition, the anti-human bFGF antibodies localized specifically to the cell, rather than to the extracellular matrix or nucleus of myotubes. The localization of bFGF demonstrated here provides further support for the hypothesis (Clegg et al., 1987; Seed et al., 1988) that this growth factor is involved in muscle development.

IGF-I increases bFGF-induced mitogenesis and upregulates FGFR-1 in rabbit vascular smooth muscle cells

1996 ◽  
Vol 270 (4) ◽  
pp. H1141-H1148 ◽  
Author(s):  
T. J. Reape ◽  
J. M. Kanczler ◽  
J. P. Ward ◽  
C. R. Thomas
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Fibroblast Growth Factor ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Fibroblast Growth ◽  
Igf I

Insulin-like growth factor-I (IGF-I) and basic fibroblast growth factor (bFGF) have both been implicated in the abnormal proliferation of vascular smooth muscle cells (VSMC) that occurs after injury to the arterial wall in vivo. We have investigated the effects of these growth factors on proliferation of rabbit aortic smooth muscle cells (RASMC) in vitro. IGF-I, in contrast to bFGF, is a weak mitogen for RASMC. However, when IGF-I (10 ng/ml) was added in combination with bFGF for 24 h, the effect of the two growth factors on DNA synthesis was synergistic at all concentrations tested (P > 0.001 compared with summed values of bFGF alone plus IGF-I alone), and this synergy was also observed at the level of RASMC proliferation (P < 0.001). Time-course experiments indicated that although bFGF was able to stimulate DNA synthesis after 16 h, activity peaked at 24 h, and a synergistic response with IGF-I was not observed before 24 h. Northern blot analysis demonstrated that IGF-I (10 ng/ml) could selectively upregulate fibroblast growth factor receptor-1 (FGFR-1) mRNA 4.0 +/- 0.24-fold (P < 0.001) without a significant effect on FGFR-2, and this induction in FGFR-1 mRNA occurs in a time- and dose-dependent manner. In addition, IGF-I increases FGFR-1 protein levels in RASMC 2.7 +/- 0.12-fold (P < 0.01), as demonstrated by Western blotting, and this upregulation occurs before the peak in DNA synthesis. These results suggest that IGF-I may be capable of increasing the responsiveness of VSMC to bFGF through modulation of FGFR-1.

Loss of fibroblast growth factor receptors is necessary for terminal differentiation of embryonic limb muscle

Development ◽  
1996 ◽  
Vol 122 (1) ◽  
pp. 291-300 ◽  
Author(s):  
N. Itoh ◽  
T. Mima ◽  
T. Mikawa
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Muscle Mass ◽  
Terminal Differentiation ◽  
Limb Bud ◽  
Fibroblast Growth ◽  
Limb Muscle ◽  
Fgf Signaling ◽  
Myotomal Muscle

Early in embryogenesis, precursors of the limb musculature are generated in the somite, migrate to the limb buds and undergo terminal differentiation. Although myogenic differentiation in culture is affected by several growth factors including fibroblast growth factor (FGF), it remains uncertain whether migration and differentiation of myogenic cells in vivo are directly regulated by such growth factors. To investigate the roles of FGF signaling in the regulation of myogenesis both in the somite and the limb bud, mosaic chicken embryos were generated that consist of somitic cells carrying transgenes expressing one of the following: FGF1, FGF4, the FGF receptor type-1 (FGFR1) or its dominant negative mutant (delta FGFR1). Cells infected with virus producing FGF ligand migrated into the somatopleure without differentiating into myotomal muscle, but differentiated into muscle fibers when they arrived in the limb bud. In contrast, cells overexpressing FGFR1 migrated into the limb muscle mass but remained as undifferentiated myoblasts. Cells infected with the delta FGFR1-producing virus failed to migrate to the somatopleure but were capable of differentiating into myotomal muscle within the somites. These results suggest that the FGFR-mediated FGF signaling (1) blocks terminal differentiation of myogenic cells within the somite and (2) sustains myoblast migration to limb buds from the somite, and that (3) down-regulation of FGFRs or FGFR signaling is involved in mechanisms triggering terminal differentiation of the limb muscle mass during avian embryogenesis.

scholarly journals Supra-Additive Expression of Interleukin-6, Interleukin-8 and Basic Fibroblast Growth Factor in Vascular Smooth Muscle Cells Following Coinfection withChlamydia pneumoniaeand Cytomegalovirus as a Novel Link between Infection and Atherosclerosis

2012 ◽  
Vol 23 (2) ◽  
pp. e26-e30 ◽  
Author(s):  
Dirk Prochnau ◽  
Eberhard Straube ◽  
Hans-Reiner Figulla ◽  
Jürgen Rödel
Keyword(s):  
Smooth Muscle ◽  
Growth Factors ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Muscle Cells ◽  
Multiple Infections ◽  
Fibroblast Growth ◽  
Increased Risk

BACKGROUND:Chlamydia pneumoniaeand human cytomegalovirus (HCMV) may be involved in the pathogenesis of atherosclerosis. Prospective studies indicate an increased risk for cardiovascular events in patients with evidence of multiple infections.OBJECTIVE: To determine whether there is a synergistic effect of coinfection withC pneumoniaeand HCMV on expression of selected growth factors and cytokines.METHODS: The production of interleukin (IL)-6, IL-8, basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), and ‘regulated on activation normal T-cell expressed and secreted’ (RANTES) was measured in coinfected aortic smooth muscle cells (AoSMC).RESULTS: Using reverse transcription polymerase chain reaction and immunoassays, it was demonstrated that the expression of IL-6, IL-8, RANTES and bFGF was stimulated in a dose- and time-dependent fashion inC pneumoniaeand also in HCMV-infected cultures. In contrast, the expression of PDGF-AA was only stimulated following HCMV infection. Coinfection withC pneumoniaeand HCMV resulted in a supra-additive stimulation of IL-6 (30% increased expression, P≤0.05) at 48 h, IL-8 (137% increased expression, P≤0.001) at 24 h and bFGF (209% increased expression, P≤0.01) at 48 h following infection.CONCLUSIONS: The findings of the present study show thatC pneumoniaeand HCMV are able to act in synergy in coinfected AoSMC. The supra-additive induction of AoSMC growth factors and cytokines indicates a novel molecular link between infection and vascular disease development.

scholarly journals Effects of prolonged infusion of basic fibroblast growth factor and IGF-I on adrenocortical differentiation in the autotransplanted adrenal: an immunohistochemical study

1999 ◽  
Vol 162 (1) ◽  
pp. 21-29 ◽  
Author(s):  
P Vendeira ◽  
D Pignatelli ◽  
D Neves ◽  
MM Magalhaes ◽  
MC Magalhaes ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Plasma Renin Activity ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Fibroblast Growth ◽  
Igf I

Adrenocortical regeneration after adrenal autotransplantation provides a model for the study of local autocrine/paracrine mechanisms involved in the growth and differentiation of the adrenal cortex. To study the possible involvement of some growth factors, namely basic fibroblast growth factor (bFGF, FGF-2) and insulin-like growth factor I (IGF-I), in cell differentiation, immunohistochemical and ultrastructural studies were carried out on adrenal autotransplants in adult male rats. To distinguish between fasciculata and glomerulosa-like cells with accuracy, tissue sections were immunostained with IZAb, which recognizes the inner zone antigen (IZAg) present in fasciculata and reticularis cells but absent from the glomerulosa, and by electron microscopy. IGF-I-treated animals exhibited a clear glomerulosa-like zone that was devoid of IZAb immunostaining. In this outer subcapsular area, ultrastructural examination showed cells containing mitochondria with irregular cristae resembling those of the fetal or immature glomerulosa cells. In contrast, no significant morphological differences were observed in bFGF-treated animals when compared with those from saline-treated controls, in both of which, IZAb immunostaining occurred in almost all adrenocortical cells, with no clear zonation or glomerulosa, as seen in the intact animal. Plasma aldosterone and corticosterone concentrations were lower in autotransplanted control animals than in intact controls, although plasma renin activities were similar. IGF-I treatment significantly increased aldosterone concentrations, whereas corticosterone and plasma renin activity were reduced. bFGF infusion further reduced plasma aldosterone, although plasma renin activity and corticosterone were unaffected. These results suggest that the two growth factors have different effects on zonal differentiation and function in the autotransplanted gland. In particular, bFGF, by reducing glomerulosa function, appears partly to replicate the actions of ACTH in normal animals. In contrast, IGF-I enhances the glomerulosa secreting phenotype and diminishes that of the fasciculata/reticularis, possibly replicating the actions of angiotensin II or a low sodium diet.

Nitric oxide selectively amplifies FGF-2-induced mitogenesis in primary rat aortic smooth muscle cells

1994 ◽  
Vol 267 (3) ◽  
pp. H1040-H1048 ◽  
Author(s):  
A. Hassid ◽  
H. Arabshahi ◽  
T. Bourcier ◽  
G. S. Dhaunsi ◽  
C. Matthews
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Fibroblast Growth Factor ◽  
Thymidine Incorporation ◽  
Muscle Cells ◽  
Fibroblast Growth ◽  
Aortic Smooth Muscle

Fibroblast growth factor is present in blood vessels and is thought to play an important role in promoting vascular cell proliferation in vivo. In the current study, we show that three agents that activate the guanosine 3',5'-cyclic monophosphate (cGMP) system, including the nitric oxide-generating agents S-nitroso-N-acetylpenicillamine (SNAP) and 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1) as well as the stable cGMP analogue 8-bromo-cGMP, increased fibroblast growth factor-2 (FGF-2; basic fibroblast growth factor)-induced [3H]thymidine incorporation by severalfold in primary cultures of rat aortic smooth muscle cells. SNAP increased the efficacy, but not the potency, of FGF-2. The stimulatory effect of SNAP was selective for FGF-2-induced mitogenesis as shown by the lack of a significant effect on [3H]thymidine incorporation induced by several other growth factors. Consistent with thymidine incorporation experiments, SNAP amplified the increase of the cellular DNA content induced by FGF-2 as well as the proliferation of cells. A selective inhibitor of cGMP phosphodiesterases, zaprinast, potentiated the comitogenic effect of SNAP and its ability to increase cGMP levels, supporting the involvement of cGMP as second messenger. Consistent with previous results, and opposite to that found in primary and early subculture, SNAP decreased mitogen-induced [3H]thymidine incorporation in cells in later subculture. Because macrophage- and vascular smooth muscle-derived nitric oxide is likely to be present in relatively large concentrations after vascular injury, we speculate that endogenous nitric oxide may amplify the activity of FGF-2 in vivo.

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