Opposite effects of monokines (interleukin-1 and tumor necrosis factor) on proliferation and heparin-binding (fibroblast) growth factor binding to human aortic endothelial and smooth muscle cells

1990 ◽  
Vol 26 (2) ◽  
pp. 213-216 ◽  
Author(s):  
Hidekazu Sawada ◽  
Mikio Kan ◽  
Wallace L. Mc Keehan
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Smooth Muscle Cells ◽  
Fibroblast Growth Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Fibroblast Growth ◽  
Heparin Binding ◽  
Necrosis Factor

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.

scholarly journals Structural Basis and Targeting of the Interaction between Fibroblast Growth Factor-inducible 14 and Tumor Necrosis Factor-like Weak Inducer of Apoptosis

2013 ◽  
Vol 288 (45) ◽  
pp. 32261-32276 ◽  
Author(s):  
Harshil Dhruv ◽  
Joseph C. Loftus ◽  
Pooja Narang ◽  
Joachim L. Petit ◽  
Maureen Fameree ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Fibroblast Growth Factor ◽  
Tumor Necrosis ◽  
Structural Basis ◽  
Fibroblast Growth ◽  
Necrosis Factor
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