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1 September 2000 Activation of Nuclear Factor κB and Induction of Apoptosis by Tumor Necrosis Factor-α in the Mouse Uterine Epithelial WEG-1 Cell Line
Serge Pampfer, Sabine Cordi, Stefan Cikos, Benjamin Picry, Ivo Vanderheyden, René De Hertogh
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Abstract

In order to better understand how tumor necrosis factor (TNF)-α may contribute to the local regulation of uterine cell death, cultures of mouse uterine epithelial WEG-1 cells were exposed to TNF-α and observed at different time intervals. Earliest decrease in cell viability was observed after 31 h of exposure to 50 ng/ml mouse TNF-α and was associated with the expression of several markers of apoptosis. Treatment with human TNF-α or addition of a neutralizing antibody against TNF-α receptor protein 80 to mouse TNF-α resulted in attenuated induction of apoptosis, suggesting that coengagement of the two TNF-α receptor types is required for maximal impact. Ceramide analogs failed to replicate the effect of TNF-α and the stress-activated protein kinase signaling pathway was not activated by the cytokine. Treatment with mouse TNF-α resulted in an increase in nuclear factor (NF)κB activity that receded after 24 h. The impact of human TNF-α on NFκB activation was more moderate. Addition of either one of three different inhibitors of NFκB (SN50, PDTC, and A771726) to mouse TNF-α sensitized WEG-1 cells to the toxicity of the cytokine. Our data suggest that WEG-1 cells initiate their response to TNF-α with an increase in NFκB activation that may have transiently biased these cells toward cell death resistance.

Serge Pampfer, Sabine Cordi, Stefan Cikos, Benjamin Picry, Ivo Vanderheyden, and René De Hertogh "Activation of Nuclear Factor κB and Induction of Apoptosis by Tumor Necrosis Factor-α in the Mouse Uterine Epithelial WEG-1 Cell Line," Biology of Reproduction 63(3), 879-886, (1 September 2000). https://doi.org/10.1095/biolreprod63.3.879
Received: 22 February 2000; Accepted: 1 April 2000; Published: 1 September 2000
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KEYWORDS
Apoptosis
cytokines
signal transduction
uterus
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