Regulation and action of fibroblast growth factor 17 in bovine follicles

Machado, Marcela Aparecida Guerreiro; Portela, Valério Marques; Price, Christopher A.; Costa, Isabela Bazzo; Ripamonte, Paula; Amorim, Renée Laufer; Buratini, J.

doi:10.1677/joe-09-0145

Cited by 52 publications

(26 citation statements)

References 44 publications

(23 reference statements)

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Section: The Role Of the Fgf8 Family In Follicle Developmentmentioning

confidence: 63%

“…FGF17 mRNA was detected mainly in oocytes with trace amounts in granulosa and theca cells (Machado et al 2009), which is not dissimilar to the pattern of expression of FGF8 mRNA in this species. FGF17 protein was readily detected in oocytes and granulosa cells; addition of recombinant FGF17 to granulosa cells in vitro inhibited oestradiol and progesterone secretion (Machado et al 2009). Similarly to FGF8, the restricted pattern of expression of FGF17 to the oocyte led to studies of a potential action in cumulus oocyte communication; addition of FGF17 increased the proportion of bovine COCs that fully expanded, but this did not improve the developmental competence of the oocyte (Machado et al 2015).…”

Section: The Role Of the Fgf8 Family In Follicle Developmentmentioning

confidence: 63%

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Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Price

2015

Journal of Endocrinology

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Fibroblast growth factors (FGFs) have been shown to alter growth and differentiation of reproductive tissues in a variety of species. Within the female reproductive tract, the effects of FGFs have been focused on the ovary, and the most studied one is FGF2, which stimulates granulosa cell proliferation and decreases differentiation (decreased steroidogenesis). Other FGFs have also been implicated in ovarian function, and this review summarizes the effects of members of two subfamilies on ovarian function; the FGF7 subfamily that also contains FGF10, and the FGF8 subfamily that also contains FGF18. There are data to suggest that FGF8 and FGF18 have distinct actions on granulosa cells, despite their apparent similar receptor binding properties. Studies of non-reproductive developmental biology also indicate that FGF8 is distinct from FGF18, and that FGF7 is also distinct from FGF10 despite similar receptor binding properties. In this review, the potential mechanisms of differential action of FGF7/FGF10 and FGF8/FGF18 during organogenesis will be reviewed and placed in the context of follicle development. A model is proposed in which FGF8 and FGF18 differentially activate receptors depending on the properties of the extracellular matrix in the follicle.

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Section: The Role Of the Fgf8 Family In Follicle Developmentmentioning

confidence: 63%

Section: The Role Of the Fgf8 Family In Follicle Developmentmentioning

confidence: 63%

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Price

2015

Journal of Endocrinology

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“…Treatment with FGF7 reduced basal and FSH-stimulated levels of granulosa cell CYP19A1 activity in vitro (Parrott & Skinner 1998). A similar antisteroidogenic effect was attributed to FGF17, which increases significantly in granulosa and theca cells from atretic follicles (Machado et al 2009) and is negatively regulated by FSH and IGF1. Recently, Portela et al (2010) demonstrated that FGF18 from theca cells is involved in follicle atresia.…”

Section: Introductionmentioning

confidence: 73%

FGF10 inhibits dominant follicle growth and estradiol secretion in vivo in cattle

Gasperin

Ferreira²,

Rovani³

et al. 2012

Reproduction

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Fibroblast growth factors (FGFs) are involved in paracrine control of follicle development. It was previously demonstrated that FGF10 decreases estradiol (E 2 ) secretion in granulosa cell culture and that theca cell FGF10 mRNA expression is decreased in healthy follicles from abattoir ovaries. The main objectives of this study were to evaluate FGF10 and FGFR2b mRNA expression during follicular development in vivo, to evaluate the effect of FGF10 on follicle growth using Bos taurus taurus cows as a model, and to gain more insight into the mechanisms through which FGF10 inhibits steroidogenesis. Messenger RNA encoding both FGF10 and FGFR2b (main FGF10 receptor) was significantly more expressed in subordinate follicles (SFs) than in dominant follicles (DFs). The intrafollicular injection of FGF10 into the largest growing follicle at 7-8 mm in diameter interrupted the DF growth in a dose-dependent manner (11G0.4, 8.3G1 and 5.9G0.3 mm for 0, 0.1, and 1 mg/ml FGF10, respectively, at 72 h after treatment; P!0.05). In a third experiment, follicles were obtained 24 h after FGF10 (1 mg/ml) or PBS treatment through ovariectomy. In theca cells, FGF10 treatment did not affect mRNA encoding steroidogenic enzymes, LHCGR and IGFBPs, but significantly upregulated FGF10 mRNA expression. The expression of CYP19A1 mRNA in granulosa cells was downregulated by FGF10 treatment, which was accompanied by a 50-fold decrease in E 2 production, and decreased cyclin D2 mRNA. These results have shown that FGF10 and its receptor FGFR2b are more expressed in SFs and provide solid in vivo evidence that FGF10 acts as an important regulator of follicular growth in cattle.

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“…Indeed, in the liver, the major target tissue of FGF19, FGF18 protein is coexpressed with ␤Klotho (2, 32), and similarly, in the kidney, the major target tissue of FGF23, FGF17 protein is coexpressed with ␣Klotho (35,60,68). Protein coexpression of FGF8 subfamily ligands and Klotho coreceptors also occurs in mature ovarian follicles (35,38,56) and in breast tissue (64,72,76). It should also be noted that other paracrine FGFs, including ligands of the FGF4 and FGF9 subfamilies, also coexist with ␣/␤Klotho coreceptors in target tissues of endocrine FGFs such as pancreas (17) and adipose tissue (13).…”

Section: Discussionmentioning

confidence: 99%

Klotho Coreceptors Inhibit Signaling by Paracrine Fibroblast Growth Factor 8 Subfamily Ligands

Goetz

Ohnishi

Ding

et al. 2012

Molecular and Cellular Biology

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e It has been recently established that Klotho coreceptors associate with fibroblast growth factor (FGF) receptor tyrosine kinases (FGFRs) to enable signaling by endocrine-acting FGFs. However, the molecular interactions leading to FGF-FGFR-Klotho ternary complex formation remain incompletely understood. Here, we show that in contrast to ␣Klotho, ␤Klotho binds its cognate endocrine FGF ligand (FGF19 or FGF21) and FGFR independently through two distinct binding sites. FGF19 and FGF21 use their respective C-terminal tails to bind to a common binding site on ␤Klotho. Importantly, we also show that Klotho coreceptors engage a conserved hydrophobic groove in the immunoglobulin-like domain III (D3) of the "c" splice isoform of FGFR. Intriguingly, this hydrophobic groove is also used by ligands of the paracrine-acting FGF8 subfamily for receptor binding. Based on this binding site overlap, we conclude that while Klotho coreceptors enhance binding affinity of FGFR for endocrine FGFs, they actively suppress binding of FGF8 subfamily ligands to FGFR. Fibroblast growth factor (FGF) signaling plays pleiotropic roles in metazoan development and metabolism (5, 24). Based on sequence homology and phylogenetic and structural considerations, the 18 mammalian FGF ligands are grouped into five paracrine-acting subfamilies and one endocrine-acting subfamily comprising FGF19, FGF21, and FGF23 (24,43). Paracrine FGFs have high affinity for pericellular heparan sulfate (HS) glycosaminoglycans (3, 5) and form distinct morphogenetic gradients in the pericellular matrix (27, 39) to fulfill essential roles during embryonic development (7,24,65). In contrast, endocrine FGFs exhibit poor affinity for HS (3, 15) and thus are able to enter the blood circulation to regulate key metabolic processes, including bile acid homeostasis (18,20,36) and hepatic glucose and protein metabolism (30, 57) (FGF19), glucose and lipid metabolism (4, 21, 29, 58) (FGF21), and vitamin D and phosphate homeostasis (1, 59, 62) (FGF23). These hormone-like FGFs have taken center stage in drug discovery for a number of inherited and acquired metabolic disorders (5, 6).Mammalian FGFs signal through four FGF receptor (FGFR) tyrosine kinases (FGFR1 to FGFR4) and their alternatively spliced isoforms (23, 43). The extracellular domain of a prototypical FGFR consists of three immunoglobulin-like domains (D1 to D3), and structural and biochemical studies have established that the region including D2, D3, and the D2-D3 linker comprises the minimal ligand-binding domain (54,55,63). The ligand-binding specificity of FGFR1 to FGFR3 is primarily regulated by a tissuespecific splicing in D3 of these receptors that generates "b" and "c" isoforms (9,26,42,52). Structural studies have revealed that this splicing alters the primary amino acid sequence of key ligandbinding loops/pockets in D3 (50,74).In addition to mediating paracrine FGF gradient formation in the pericellular matrix, HS is required for enhancing the affinity of paracrine FGF for FGFR and promoting dimerization of ligan...

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Regulation and action of fibroblast growth factor 17 in bovine follicles

Cited by 52 publications

References 44 publications

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

Mechanisms of fibroblast growth factor signaling in the ovarian follicle

FGF10 inhibits dominant follicle growth and estradiol secretion in vivo in cattle

Klotho Coreceptors Inhibit Signaling by Paracrine Fibroblast Growth Factor 8 Subfamily Ligands

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