scholarly journals Fibroblast growth factor 23 mRNA expression profile in chickens and its response to dietary phosphorus

2018 ◽  
Vol 97 (7) ◽  
pp. 2258-2266 ◽  
Author(s):  
R.M. Wang ◽  
J.P. Zhao ◽  
X.J. Wang ◽  
H.C. Jiao ◽  
J.M. Wu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Expression Profile ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Mrna Expression Profile ◽  
Dietary Phosphorus

scholarly journals Effects of gender and body weight on fibroblast growth factor 23 responsiveness to estimated dietary phosphorus

2016 ◽  
Vol 63 (1.2) ◽  
pp. 58-62 ◽  
Author(s):  
Hiroyuki Ohta ◽  
Masae Sakuma ◽  
Akitsu Suzuki ◽  
Yuuka Morimoto ◽  
Makoto Ishikawa ◽  
...  
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Dietary Phosphorus

Fibroblast growth factor 23 production in bone is directly regulated by 1α,25-dihydroxyvitamin D, but not PTH

2010 ◽  
Vol 299 (5) ◽  
pp. F1212-F1217 ◽  
Author(s):  
Fumie Saji ◽  
Takashi Shigematsu ◽  
Toshifumi Sakaguchi ◽  
Masaki Ohya ◽  
Hikari Orita ◽  
...  
Keyword(s):  
Growth Factor ◽  
Renal Insufficiency ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
Dihydroxyvitamin D ◽  
Fgf23 Concentration ◽  
Group A

Fibroblast growth factor 23 (FGF23), which is primarily produced by osteocytes in bone, regulates renal phosphate excretion and 1α,25-dihydroxyvitamin D [1,25(OH)2D3] metabolism. Patients with chronic kidney disease (CKD) have increased levels of circulating serum FGF23, but the direct effect on circulating FGF23 levels in renal insufficiency is still unclear. To identify the major regulator of FGF23 synthesis in renal insufficiency, we compared the effect of parathyroid hormone (PTH) and 1,25(OH)2D3 on FGF23 synthesis in the calvariae of normal rats with that of uremic rats in vitro. 1,25(OH)2D3 treatment significantly increased the FGF23 concentration in the medium from both groups, but the degree of increase in the uremic group was markedly higher than in the control group. A significant increase in FGF23 mRNA expression occurred as early as 4 h after treatment and reached the maximum within 8 h in the uremic group, whereas in the normal group a significant increase in FGF23 mRNA expression was observed only at 8 h. In addition, the expression of vitamin D receptor (VDR) mRNA in the calvariae of uremic rats was markedly higher than in normal rats. However, in neither group did PTH treatment affect the medium FGF23 concentration or the FGF23 mRNA levels. These results suggest that FGF23 synthesis in bone is regulated by 1,25(OH)2D3 directly, not by PTH, and that increased VDR mRNA expression induced the relatively swift and strong response in the uremic group.

scholarly journals 1α,25-dihydroxyvitamin D3 acts predominately in mature osteoblasts under conditions of high extracellular phosphate to increase fibroblast growth factor 23 production in vitro

2010 ◽  
Vol 206 (3) ◽  
pp. 279-286 ◽  
Author(s):  
Ryoko Yamamoto ◽  
Tomoko Minamizaki ◽  
Yuji Yoshiko ◽  
Hirotaka Yoshioka ◽  
Kazuo Tanne ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Prostaglandin E ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
Dihydroxyvitamin D3 ◽  
Osteoblast Development

Osteoblasts/osteocytes are the principle sources of fibroblast growth factor 23 (FGF23), a phosphaturic hormone, but the regulation of FGF23 expression during osteoblast development remains uncertain. Because 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) and inorganic phosphate (Pi) may act as potent activators of FGF23 expression, we estimated how these molecules regulate FGF23 expression during rat osteoblast development in vitro. 1,25(OH)2D3-dependent FGF23 production was restricted largely to mature cells in correlation with increased vitamin D receptor (VDR) mRNA levels, in particular, when Pi was present. Pi alone and more so in combination with 1,25(OH)2D3 increased FGF23 production and VDR mRNA expression. Parathyroid hormone, stanniocalcin 1, prostaglandin E2, FGF2, and foscarnet did not increase FGF23 mRNA expression. Thus, these results suggest that 1,25(OH)2D3 may exert its largest effect on FGF23 expression/production when exposed to high levels of extracellular Pi in osteoblasts/osteocytes.

scholarly journals Sclerostin directly stimulates osteocyte synthesis of fibroblast growth factor-23

2020 ◽  
Author(s):  
Nobuaki Ito ◽  
Matthew Prideaux ◽  
Asiri R. Wijenayaka ◽  
Dongqing Yang ◽  
Renee T. Ormsby ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Cell Model ◽  
Ex Vivo ◽  
Fibroblast Growth Factor 23 ◽  
Mrna Levels ◽  
Fibroblast Growth ◽  
Pi Homeostasis

AbstractOsteocyte produced fibroblast growth factor 23 (FGF23) is the key regulator of serum phosphate (Pi) homeostasis. The interplay between parathyroid hormone (PTH), FGF23 and other proteins that regulate FGF23 production and serum Pi levels is complex and incompletely characterised. Evidence suggests that the protein product of the SOST gene, sclerostin (SCL), also a PTH target and also produced by osteocytes, plays a role in FGF23 expression, however the mechanism for this effect is unclear. Part of the problem of understanding the interplay of these mediators is the complex multi-organ system that achieves Pi homeostasis in vivo. In the current study, we sought to address this using a unique cell line model of the osteocyte, IDG-SW3, known to express FGF23 at both the mRNA and protein levels. In cultures of differentiated IDG-SW3 cells, both PTH1-34 and recombinant human (rh) SCL remarkably induced Fgf23 mRNA expression dose-dependently within 3 hours. Both rhPTH1-34 and rhSCL also strongly induced C-terminal FGF23 protein secretion. Secreted intact FGF23 levels remained unchanged, consistent with constitutive post-translational cleavage of FGF23 in this cell model. Both rhPTH1-34 and rhSCL treatments significantly suppressed mRNA levels of Phex, Dmp1 and Enpp1 mRNA, encoding putative negative regulators of FGF23 levels, and induced Galnt3 mRNA expression, encoding N-acetylgalactosaminyl-transferase 3 (GalNAc-T3), which protects FGF23 from furin-like proprotein convertase-mediated cleavage. The effect of both rhPTH1-34 and rhSCL was antagonised by pre-treatment with the NF-κβ signalling inhibitors, BAY11 and TPCK. RhSCL also stimulated FGF23 mRNA expression in ex vivo cultures of human bone. These findings provide evidence for the direct regulation of FGF23 expression by sclerostin. Locally expressed sclerostin via the induction of FGF23 in osteocytes thus has the potential to contribute to the regulation of Pi homeostasis.

Sex and iron modify fibroblast growth factor 23 concentrations in 1-year-old children

2017 ◽  
Author(s):  
Elisa Holmlund-Suila ◽  
Maria Enlund-Cerullo ◽  
Saara Valkama ◽  
Helena Hauta-alus ◽  
Jenni Rosendahl ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth
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