scholarly journals Prostate tumorigenesis in estrogen receptor [beta] inactivated, prostate targeted fibroblast growth factor 8B transgenic mice

2013 ◽  
Author(s):  
Teresa Elo ◽  
Lan Yu ◽  
Eeva Valve ◽  
Sari Makela ◽  
Pirkko Harkonen
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Fibroblast Growth Factor ◽  
Estrogen Receptor Beta ◽  
Fibroblast Growth ◽  
Prostate Tumorigenesis ◽  
Receptor Beta

scholarly journals Transgenic Mice Overexpressing Human Fibroblast Growth Factor 23 (R176Q) Delineate a Putative Role for Parathyroid Hormone in Renal Phosphate Wasting Disorders

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5269-5279 ◽  
Author(s):  
Xiuying Bai ◽  
Dengshun Miao ◽  
Jiarong Li ◽  
David Goltzman ◽  
Andrew C. Karaplis
Keyword(s):  
Vitamin D ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Fibroblast Growth Factor ◽  
Calcium Homeostasis ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Vitamin D Metabolism ◽  
Dihydroxyvitamin D3 ◽  
Circulating Levels

Abstract Fibroblast growth factor 23 (FGF23) is a recently characterized protein likely involved in the regulation of serum phosphate homeostasis. Increased circulating levels of FGF23 have been reported in patients with renal phosphate-wasting disorders, but it is unclear whether FGF23 is the direct mediator responsible for the decreased phosphate transport at the proximal renal tubules and the altered vitamin D metabolism associated with these states. To examine this question, we generated transgenic mice expressing and secreting from the liver human FGF23 (R176Q), a mutant form that fails to be degraded by furin proteases. At 1 and 2 months of age, mice carrying the transgene recapitulated the biochemical (decreased urinary phosphate reabsorption, hypophosphatemia, low serum 1,25-dihydroxyvitamin D3) and skeletal (rickets and osteomalacia) alterations associated with these disorders. Unexpectantly, marked changes in parameters of calcium homeostasis were also observed, consistent with secondary hyperparathyroidism. Moreover, in the kidney the anticipated alterations in the expression of hydroxylases associated with vitamin D metabolism were not observed despite the profound hypophosphatemia and increased circulating levels of PTH, both major physiological stimuli for 1,25-dihydroxyvitamin D3 production. Our findings strongly support the novel concept that high circulating levels of FGF23 are associated with profound disturbances in the regulation of phosphate and vitamin D metabolism as well as calcium homeostasis and that elevated PTH levels likely also contribute to the renal phosphate wasting associated with these disorders.

Accelerated fracture healing in transgenic mice overexpressing an anabolic isoform of fibroblast growth factor 2

2016 ◽  
Vol 117 (3) ◽  
pp. 599-611 ◽  
Author(s):  
Marja M. Hurley ◽  
Douglas J. Adams ◽  
Liping Wang ◽  
Xi Jiang ◽  
Patience Meo Burt ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Fracture Healing ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth

scholarly journals Klotho/fibroblast growth factor 23- and PTH-independent estrogen receptor-α-mediated direct downregulation of NaPi-IIa by estrogen in the mouse kidney

2016 ◽  
Vol 311 (2) ◽  
pp. F249-F259 ◽  
Author(s):  
Rose Webster ◽  
Sulaiman Sheriff ◽  
Rashma Faroqui ◽  
Faraaz Siddiqui ◽  
John R. Hawse ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Food Intake ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Estrogen Receptor Α ◽  
Estrogen Treatment ◽  
Fibroblast Growth ◽  
Reading Frame ◽  
Receptor Isoforms

Estrogen treatment causes renal phosphate (Pi) wasting and hypophosphatemia in rats and humans; however, the signaling mechanisms mediating this effect are still poorly understood. To determine the specific roles of estrogen receptor isoforms (ERα and ERβ) and the Klotho pathway in mediating these effects, we studied the effects of estrogen on renal Pi handling in female mice with null mutations of ERα or ERβ or Klotho and their wild type (WT) using balance studies in metabolic cages. Estrogen treatment of WT and ERβ knockout (KO) mice caused a significant reduction in food intake along with increased renal phosphate wasting. The latter resulted from a significant downregulation of NaPi-IIa and NaPi-IIc protein abundance. The mRNA expression levels of both transporters were unchanged in estrogen-treated mice. These effects on both food intake and renal Pi handling were absent in ERα KO mice. Estrogen treatment of Klotho KO mice or parathyroid hormone (PTH)-depleted thyroparathyroidectomized mice exhibited a significant downregulation of NaPi-IIa with no change in the abundance of NaPi-IIc. Estrogen treatment of a cell line (U20S) stably coexpressing both ERα and ERβ caused a significant downregulation of NaPi-IIa protein when transiently transfected with a plasmid containing full-length or open-reading frame (ORF) 3′-untranslated region (UTR) but not 5′-UTR ORF of mouse NaPi-IIa transcript. In conclusion, estrogen causes phosphaturia and hypophosphatemia in mice. These effects result from downregulation of NaPi-IIa and NaPi-IIc proteins in the proximal tubule through the activation of ERα. The downregulation of NaPi-IIa by estrogen involves 3′-UTR of its mRNA and is independent of Klotho/fibroblast growth factor 23 and PTH signaling pathways.

FGF-2 Dependent Angiogenesis is a Latent Phenotype in Basic Fibroblast Growth Factor Transgenic Mice

Endothelium ◽  
1999 ◽  
Vol 6 (3) ◽  
pp. 185-195 ◽  
Author(s):  
D.-L. Fulgham ◽  
S.-R. Widhalm ◽  
S. Martin ◽  
J.-D. Coffin
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Fibroblast Growth

Detection and Characterization of Estrogen Receptor Beta Expression in the Brain with Newly Developed Transgenic Mice

Neuroscience ◽  
2020 ◽  
Vol 438 ◽  
pp. 182-197
Author(s):  
Shoko Sagoshi ◽  
Sho Maejima ◽  
Masahiro Morishita ◽  
Satoshi Takenawa ◽  
Akito Otubo ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Transgenic Mice ◽  
Estrogen Receptor Beta ◽  
The Brain ◽  
Receptor Beta
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