Sulindac suppresses nuclear factor-kappaB activation and RANTES gene and protein expression in endometrial stromal cells from women with endometriosis

Fritz Wieser, Wieser F, Jean‐Louis Vigne, Jean-Louis Vigne, Vigne JL, Isabelle P. Ryan, Ryan I, Isabelle Ryan, Hornung D, Daniela Hornung, Schima Djalali, Djalali S, Robert N. Taylor, Taylor RN
The Journal of clinical endocrinology and metabolism · 2005 · vol. 90(12) , pp. 6441–6447 · doi:10.1210/jc.2005-0972 · PMID:16159934 · W2068896914
Lab / animal OA: bronze CC0 ⤵ 44 in-corpus citations
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Sulindac suppressed nuclear factor-κB activation and RANTES gene and protein expression in endometrial stromal cells from women with endometriosis.

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Abstract

CONTEXT: The nuclear factor-kappaB (NF-kappaB) pathway is a critical mediator of RANTES (regulated on activation, normal T cell expressed and secreted) gene regulation and therefore represents a potential target for therapy of endometriosis-associated symptoms. OBJECTIVE: The objective of this study was to investigate the effects of the antiinflammatory drug sulindac on NF-kappaB activation, NF-kappaB-mediated gene expression, RANTES gene and protein expression in endometrial stromal cells isolated from women with endometriosis, and unaffected controls. DESIGN: This was a clinical experimental study. SETTING: The study was conducted at a university hospital. RESULTS: The inflammatory response in endometriosis is augmented by a 5-fold increased TNFalpha-induced RANTES secretion from ectopic endometriotic stromal cells, compared with normal endometrial stromal cells (P < 0.05). Western blot analysis revealed basal activation of NF-kappaB in endometriotic cells, which could be suppressed by sulindac. EMSAs showed that sulindac dramatically decreased NF-kappaB activation and diminished TNFalpha and IL-1beta-induced NF-kappaB DNA binding activity. Sulindac pretreatment resulted in a significant decrease in TNFalpha-induced luciferase activity of NF-kappaB response element and -477 bp RANTES promoter constructs in normal and endometriotic stromal cells. The addition of sulindac to IL-1beta- and TNFalpha-treated endometriotic stromal cells also resulted in a 4-fold inhibition of RANTES protein secretion (P < 0.05). CONCLUSIONS: We have demonstrated that sulindac exerts strong antiinflammatory effects by suppression of NF-kappaB translocation, inhibition of NF-kappaB-mediated gene transcription, RANTES gene expression, and protein secretion in normal and endometriotic stromal cells. These results suggest that drugs targeting the NF-kappaB pathway may be beneficial in the treatment of endometriosis-associated symptoms.

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Condition tags

endometriosis

MeSH descriptors

Anti-Inflammatory Agents, Non-Steroidal Chemokine CCL5 Endometriosis Endometrium NF-kappa B Stromal Cells Sulindac Adult Adult Anti-Inflammatory Agents, Non-Steroidal Anti-Inflammatory Agents, Non-Steroidal Biological Transport Biological Transport Biological Transport Cells, Cultured Cells, Cultured Chemokine CCL5 Chemokine CCL5 Chemokine CCL5 Endometriosis

Citation neighborhood

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