scholarly journals Functional Diversity of Fibroblast Growth Factors in Bone Formation

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Yuichiro Takei ◽  
Tomoko Minamizaki ◽  
Yuji Yoshiko
Keyword(s):  
Bone Formation ◽  
Functional Diversity ◽  
Fibroblast Growth Factors ◽  
Serum Phosphate ◽  
Negative Regulation ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Research Groups ◽  
Renal Phosphate Reabsorption ◽  
Spatiotemporal Control

The functional significance of fibroblast growth factor (FGF) signaling in bone formation has been demonstrated through genetic loss-of-function and gain-of-function approaches. FGFs, comprising 22 family members, are classified into three subfamilies: canonical, hormone-like, and intracellular. The former two subfamilies activate their signaling pathways through FGF receptors (FGFRs). Currently, intracellular FGFs appear to be primarily involved in the nervous system. Canonical FGFs such as FGF2 play significant roles in bone formation, and precise spatiotemporal control of FGFs and FGFRs at the transcriptional and posttranscriptional levels may allow for the functional diversity of FGFs during bone formation. Recently, several research groups, including ours, have shown that FGF23, a member of the hormone-like FGF subfamily, is primarily expressed in osteocytes/osteoblasts. This polypeptide decreases serum phosphate levels by inhibiting renal phosphate reabsorption and vitamin D3activation, resulting in mineralization defects in the bone. Thus, FGFs are involved in the positive and negative regulation of bone formation. In this review, we focus on the reciprocal roles of FGFs in bone formation in relation to their local versus systemic effects.

Implications of Fibroblast Growth Factors (FGFs) in Cancer: From Prognostic to Therapeutic Applications

2019 ◽  
Vol 20 (8) ◽  
pp. 852-870
Author(s):  
Hassan Dianat-Moghadam ◽  
Ladan Teimoori-Toolabi
Keyword(s):  
Growth Factors ◽  
Wound Repair ◽  
Fibroblast Growth Factors ◽  
Predictive Biomarkers ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Cellular Processes ◽  
Fgfr Signaling ◽  
Proliferation And Metastasis ◽  
Immense Potential

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.

Cytogenetics, Immunostaining for Fibroblast Growth Factors, p53 Sequencing, and Clinical Features of Two Cases of Cystosarcoma Phyllodes

2000 ◽  
Vol 5 (3) ◽  
pp. 179-190 ◽  
Author(s):  
PAUL V. WOOLLEY ◽  
SUSANNE M. GOLLIN ◽  
WAHEEB RISKALLA ◽  
SYDNEY FINKELSTEIN ◽  
DAVID F. STEFANIK ◽  
...  
Keyword(s):  
Growth Factors ◽  
Clinical Features ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Cystosarcoma Phyllodes

scholarly journals Acidic and basic fibroblast growth factors stimulate tyrosine kinase activity in vivo.

1988 ◽  
Vol 263 (2) ◽  
pp. 988-993 ◽  
Author(s):  
S R Coughlin ◽  
P J Barr ◽  
L S Cousens ◽  
L J Fretto ◽  
L T Williams
Keyword(s):  
Growth Factors ◽  
Tyrosine Kinase ◽  
Kinase Activity ◽  
Fibroblast Growth Factors ◽  
Fibroblast Growth ◽  
Tyrosine Kinase Activity

scholarly journals Protective Effects of Moderate Ca Supplementation against Cd-Induced Bone Damage under Different Population-Relevant Doses in Young Female Rats

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 849 ◽  
Author(s):  
Huang ◽  
Liu ◽  
Zhao ◽  
Fu ◽  
Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Bone Formation ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Young Female ◽  
Female Rats ◽  
Bone Biomechanics ◽  
Protective Effects ◽  
Fibroblast Growth ◽  
Bone Damage

Estimation of the skeleton-protective effects of Ca in Cd-induced bone damage is helpful in the assessment of Cd health risk. The aim of this study was to identify whether Ca supplementation during exposure to different population-relevant doses of Cd can prevent Cd-induced bone damage under the tolerable upper intake level of Ca supplementation. Young female Sprague-Dawley rats were given different population-relevant doses of Cd (1, 5, and 50 mg Cd/kg diet) and Ca supplementation (0.4% Ca supplementation) intervention. Ca supplementation significantly decreased Cd-induced bone microstructure damage, increased bone biomechanics (p < 0.05), serum bone formation marker level (p < 0.05) and expression of osteogenic gene markers exposure to the 5 and 50 mg Cd/kg diets. However, it had no impact on these indicators under the 1 mg Cd/kg diets, with the exception of expression of osteogenic marker genes. Ca supplementation significantly decreased serum Klotho level (p < 0.05), and fibroblast growth factor 23/Klotho-associated gene expression in the kidney and bone showed significant changes. In conclusion, Ca supplementation has a positive effect on bone formation and bone quality against the damaging impact of Cd, especially with exposure to the 5 mg and 50 mg Cd/kg diet, which may be related to its impact on the fibroblast growth factor 23/Klotho axis.

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