Activity of Mangosteen Xanthones and Teleocidin A-2 in Death Receptor Expression Enhancement and Tumor Necrosis Factor Related Apoptosis-Inducing Ligand Assays#

ABSTRACT Chlamydia psittaci was found to modulate receptor expression for the cytokine receptors that are involved in the synergistic induction of indoleamine dioxygenase in epithelial cells. Increases in receptor expression were seen even with inactivated Chlamydia, suggesting that chlamydial antigens and not products of infection are important for up-regulating cytokine receptor expression.

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Calyculin A causes sensitization to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by ROS-mediated down-regulation of cellular FLICE-inhibiting protein (c-FLIP) and by enhancing death receptor 4 mRNA stabilization

APOPTOSIS ◽

10.1007/s10495-012-0753-y ◽

2012 ◽

Vol 17 (11) ◽

pp. 1223-1234 ◽

Cited By ~ 12

Author(s):

Seon Min Woo ◽

Kyoung-jin Min ◽

Taeg Kyu Kwon

Keyword(s):

Tumor Necrosis Factor ◽

Protein C ◽

Tumor Necrosis ◽

Death Receptor ◽

Calyculin A ◽

Down Regulation ◽

Mrna Stabilization ◽

Induced Apoptosis ◽

Death Receptor 4 ◽

Necrosis Factor

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Tumor necrosis factor decreases thrombin receptor expression in endothelial cells

Journal of Cellular Physiology ◽

10.1002/(sici)1097-4652(199603)166:3<561::aid-jcp10>3.0.co;2-a ◽

1996 ◽

Vol 166 (3) ◽

pp. 561-567 ◽

Cited By ~ 20

Author(s):

W. Yan ◽

C. Tiruppathi ◽

R. Qiao ◽

H. Lum ◽

A. B. Malik

Keyword(s):

Endothelial Cells ◽

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Receptor Expression ◽

Thrombin Receptor ◽

Necrosis Factor

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Tumor Necrosis Factor (TNF) Receptor Expression Determines Keratinocyte Fate upon Stimulation with TNF-Like Weak Inducer of Apoptosis

Mediators of Inflammation ◽

10.1155/2019/2945083 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13 ◽

Cited By ~ 3

Author(s):

Xuening Wang ◽

Dan Cheng ◽

Guanglei Hu ◽

Lili Liang ◽

Fei Tan ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Receptor Expression ◽

Structural Basis ◽

Tnf Receptor ◽

Death Domain ◽

Independent Manner ◽

Normal Keratinocytes ◽

Apoptosis Protein ◽

Necrosis Factor

The interaction between tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) and fibroblast growth factor-inducible 14 (Fn14) regulates the fate of keratinocytes, depending on the relative expression of TNF receptor (TNFR) 1 or TNFR2. However, the precise mechanism underlying this TWEAK-mediated regulation remains unclear. The aim of this study was to provide comprehensive insight into the roles of Fn14, TNFR1/2, and other relevant molecules in the fate of keratinocytes. Further, we sought to elucidate the structural basis for the interaction of TWEAK and Fn14 in regulating cellular outcomes. Normal keratinocytes (mainly expressing TNFR1) and TNFR2-overexpressing keratinocytes were stimulated with TWEAK. Through immunoprecipitation and Western blotting of keratinocyte lysates, we elucidated the associations between Fn14, TNFR-associated factor 2 (TRAF2), cellular inhibitor of apoptosis protein 1 (cIAP1), and TNFR1/2 molecules. Additionally, we found that TRAF2 exhibited binding to Fn14, cIAP1, and TNFR1/2. Our data suggest that TWEAK induces apoptosis in normal keratinocytes and proliferation in TNFR2-overexpressing keratinocytes in a TNF-α-independent manner; however, inhibition of TRAF2 appears to reverse this effect. Interestingly, the interaction between TWEAK and Fn14 increased TNFR1-associated death domain protein and caspase-8 expression in normal keratinocytes and promoted cytoplasmic import of cIAP1 in TNFR2-overexpressing keratinocytes. In conclusion, we found that the Fn14-TRAF2-TNFR signaling axis mediates TWEAK’s regulation of the fate of keratinocytes, possibly in a manner involving the TNF-α-independent TNFR signal transduction.

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