scholarly journals Expression and effect of fibroblast growth factor 9 in bovine theca cells

2012 ◽  
Vol 215 (1) ◽  
pp. 167-175 ◽  
Author(s):  
N B Schreiber ◽  
M L Totty ◽  
L J Spicer
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Ovarian Function ◽  
Hormonal Control ◽  
Fibroblast Growth ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Factor Α ◽  
Dose Dependent ◽  
Necrosis Factor

Fibroblast growth factor 9 (FGF9) protein affects granulosa cell (GC) function but is mostly localized to theca cell (TC) and stromal cell of rat ovaries. The objectives of this study were to determine the 1) effects of FGF9 on TC steroidogenesis, gene expression, and cell proliferation; 2) mechanism of action of FGF9 on TCs; and 3) hormonal control ofFGF9mRNA expression in TCs. Bovine ovaries were collected from a local slaughterhouse and TCs were collected from large (8–22 mm) follicles and treated with various hormones in serum-free medium for 24 or 48 h. FGF9 caused a dose-dependent inhibition (P<0.05) of LH- and LH+IGF1-induced androstenedione and progesterone production. Also, FGF9 inhibited (P<0.05) LH+IGF1-induced expression ofLHCGR,CYP11A1, andCYP17A1mRNA (via real-time RT-PCR) in TCs. FGF9 had no effect (P>0.10) onSTARmRNA abundance. Furthermore, FGF9 inhibited dibutyryl cAMP-induced progesterone and androstenedione production in LH+IGF1-treated TCs. By contrast, FGF9 increased (P<0.05) the number of bovine TCs. Abundance ofFGF9mRNA in GCs and TCs was several-fold greater (P<0.05) in small (1–5 mm) vs large follicles. Tumor necrosis factor α and WNT5A increased (P<0.05) abundance ofFGF9mRNA in TCs. In summary, expression ofFGF9mRNA in TCs is developmentally and hormonally regulated. FGF9 may act as an autocrine regulator of ovarian function in cattle by slowing TC differentiation via inhibiting LH+IGF1 action via decreasing gonadotropin receptors and the cAMP signaling cascade while stimulating proliferation of TCs.

scholarly journals Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling

2017 ◽  
Vol 43 (2) ◽  
pp. 579-588 ◽  
Author(s):  
Xuening Wang ◽  
Shengxiang Xiao ◽  
Yumin Xia
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Fibroblast Growth Factor ◽  
Tumor Necrosis ◽  
Expression Profiles ◽  
Tumor Necrosis Factor Receptor ◽  
Fibroblast Growth ◽  
Cell Fates ◽  
Apoptosis Protein ◽  
Necrosis Factor

Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor–inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis.

scholarly journals Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK)/Fibroblast Growth Factor-Inducible 14 (Fn14) Axis in Cardiovascular Diseases: Progress and Challenges

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 405
Author(s):  
Nerea Méndez-Barbero ◽  
Carmen Gutiérrez-Muñoz ◽  
Rafael Blázquez-Serra ◽  
Jose Martín-Ventura ◽  
Luis Blanco-Colio
Keyword(s):  
Cardiovascular Diseases ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Fibroblast Growth Factor ◽  
Tumor Necrosis ◽  
Fibroblast Growth ◽  
Cardiovascular Remodeling ◽  
Cytokine Tumor Necrosis Factor ◽  
Artery Disease ◽  
Necrosis Factor

Cardiovascular diseases (CVD) are the leading cause of mortality in Western countries. CVD include several pathologies, such as coronary artery disease, stroke, peripheral artery disease, and aortic aneurysm, among others. All of them are characterized by a pathological vascular remodeling in which inflammation plays a key role. Interaction between different members of the tumor necrosis factor superfamily and their cognate receptors induce several biological actions that may participate in CVD. The cytokine tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), are abundantly expressed during pathological cardiovascular remodeling. The TWEAK/Fn14 axis controls a variety of cellular functions, such as proliferation, differentiation, and apoptosis, and has several biological functions, such as inflammation and fibrosis that are linked to CVD. It has been demonstrated that persistent TWEAK/Fn14 activation is involved in both vessel and heart remodeling associated with acute and chronic CVD. In this review, we summarized the role of the TWEAK/Fn14 axis during pathological cardiovascular remodeling, highlighting the cellular components and the signaling pathways that are involved in these processes.

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