Sulindac Suppresses Nuclear Factor-κB Activation and RANTES Gene and Protein Expression in Endometrial Stromal Cells from Women with Endometriosis

Fritz Wieser, Jean‐Louis Vigne, Jean-Louis Vigne, Isabelle P. Ryan, Isabelle Ryan, Daniela Hornung, Schima Djalali, Robert N Taylor
The Journal of clinical endocrinology and metabolism · 2005 · vol. 90(12) , pp. 6441–6447 · doi:10.1210/jc.2005-0972 · PMID:16159934 · W2068896914
article OA: bronze CC0 ⤵ 44 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Sulindac suppressed nuclear factor-κB activation and RANTES gene and protein expression in endometrial stromal cells from women with endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Context: The nuclear factor-κB (NF-κB) 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-κB activation, NF-κB-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 TNFα-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-κB in endometriotic cells, which could be suppressed by sulindac. EMSAs showed that sulindac dramatically decreased NF-κB activation and diminished TNFα and IL-1β-induced NF-κB DNA binding activity. Sulindac pretreatment resulted in a significant decrease in TNFα-induced luciferase activity of NF-κB response element and −477 bp RANTES promoter constructs in normal and endometriotic stromal cells. The addition of sulindac to IL-1β- and TNFα-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-κB translocation, inhibition of NF-κB-mediated gene transcription, RANTES gene expression, and protein secretion in normal and endometriotic stromal cells. These results suggest that drugs targeting the NF-κB pathway may be beneficial in the treatment of endometriosis-associated symptoms.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

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

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (53)

Cited by (44)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:15:35.797702+00:00
License: CC0 · commercial use OK