Distribution of acidic and basic fibroblast growth factors in ovine skin during follicle morphogenesis

1993 ◽  
Vol 105 (3) ◽  
pp. 667-674
Author(s):  
D.L. du Cros ◽  
K. Isaacs ◽  
G.P. Moore

Acidic and basic fibroblast growth factors (aFGF and bFGF) have been localized by immunochemistry in ovine skin during wool follicle morphogenesis. At 40 days of gestation, prior to the appearance of follicle primordia, bFGF immunoreactivity was detected in the intermediate and periderm layers of the epidermis and at the dermal-epidermal junction. Antibodies to aFGF did not bind to skin at this age. During early follicle formation, at 76 days of gestation, both FGFs were found in the epidermis and associated with the follicle primordia. Antibodies to aFGF, in particular, bound to the basal cells of the epidermis and the follicle cell aggregations. With the development of epidermal plugs, bFGF was confined to the intermediate layers of the epidermis and the dermal-epidermal junction, whereas aFGF staining was associated with the cells of the epidermis and the plugs. At 90 days, when many different stages of follicle development were in evidence, immunoreactivity for both FGFs was associated with the cells of the elongating epidermal column, particularly those adjacent to the dermal-epidermal junction. During follicle maturation, bFGF was found in the suprabasal layer of the epidermis, in the outer root sheath of the follicle and in the basement membrane zone surrounding the bulb matrix. Conversely, strong staining for aFGF was observed in the epidermis and pilary canal contiguous with the epidermis, and in cells of the upper bulb matrix of the follicle in the region of the keratogenous zone. Western blotting of extracts of mature follicles that had been isolated from the skin showed the presence of a major aFGF immunoreactive band with an apparent molecular mass of 27 kDa.(ABSTRACT TRUNCATED AT 250 WORDS)

2000 ◽  
Vol 5 (3) ◽  
pp. 179-190 ◽  
Author(s):  
PAUL V. WOOLLEY ◽  
SUSANNE M. GOLLIN ◽  
WAHEEB RISKALLA ◽  
SYDNEY FINKELSTEIN ◽  
DAVID F. STEFANIK ◽  
...  

2019 ◽  
Vol 20 (8) ◽  
pp. 852-870
Author(s):  
Hassan Dianat-Moghadam ◽  
Ladan Teimoori-Toolabi

Fibroblast growth factors (FGFs) are pleiotropic molecules exerting autocrine, intracrine and paracrine functions via activating four tyrosine kinase FGF receptors (FGFR), which further trigger a variety of cellular processes including angiogenesis, evasion from apoptosis, bone formation, embryogenesis, wound repair and homeostasis. Four major mechanisms including angiogenesis, inflammation, cell proliferation, and metastasis are active in FGF/FGFR-driven tumors. Furthermore, gain-of-function or loss-of-function in FGFRs1-4 which is due to amplification, fusions, mutations, and changes in tumor–stromal cells interactions, is associated with the development and progression of cancer. Although, the developed small molecule or antibodies targeting FGFR signaling offer immense potential for cancer therapy, emergence of drug resistance, activation of compensatory pathways and systemic toxicity of modulators are bottlenecks in clinical application of anti-FGFRs. In this review, we present FGF/FGFR structure and the mechanisms of its function, as well as cross-talks with other nodes and/or signaling pathways. We describe deregulation of FGF/FGFR-related mechanisms in human disease and tumor progression leading to the presentation of emerging therapeutic approaches, resistance to FGFR targeting, and clinical potentials of individual FGF family in several human cancers. Additionally, the underlying biological mechanisms of FGF/FGFR signaling, besides several attempts to develop predictive biomarkers and combination therapies for different cancers have been explored.


1988 ◽  
Vol 263 (2) ◽  
pp. 988-993 ◽  
Author(s):  
S R Coughlin ◽  
P J Barr ◽  
L S Cousens ◽  
L J Fretto ◽  
L T Williams

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