Endometriotic stromal cells lose the ability to regulate cell-survival signaling in endometrial epithelial cells in vitro

Zhang H, Hui Zhang, Mei Li, Mingjiang Li, Li M, X Zheng, Xiaojing Zheng, Zheng X, Ying Sun, Sun Y, Yi Sun, Zhuzhi Wen, Wen Z, Zeqing Wen, Zhao X, Xing‐Ming Zhao, Xingbo Zhao
Molecular human reproduction · 2009 · vol. 15(10) , pp. 653–663 · doi:10.1093/molehr/gap069 · PMID:19684091 · W2123107735
article OA: closed CC0 ⤵ 27 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-06 ⓘ

Ectopic endometriotic stromal cells fail to suppress pro-survival signaling pathways in epithelial cells, unlike normal stromal cells, potentially promoting lesion growth.

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

Abstract

In normal endometrium, stromal factors regulate the growth of epithelial cells. However, epithelial cells in endometriotic lesions display increased proliferation and decreased apoptosis. This work tested the hypothesis that in endometriosis stromal cells lose the ability to regulate survival signaling and cell growth in epithelial cells. Primary normal, endometriotic eutopic and ectopic epithelial cells were cultured in the presence of medium conditioned by normal, eutopic and ectopic endometriotic endometrial stromal cells. Endometriotic epithelial cells showed higher Survivin expression than normal epithelial cells. Conditioned medium (CM) from normal or eutopic endometriotic stromal cells significantly inhibited the Survivin expression and AKt phosphorylation in normal or eutopic endometriotic epithelial cells. However, CM from ectopic endometriotic stromal cells did not have an inhibitory effect on normal or ectopic endometriotic epithelial cells. Inhibition of AKt phosphorylation and Survivin expression in normal or eutopic endometriotic epithelial cells in the presence of stromal factors from normal or eutopic endometriotic stromal cells was enhanced by progesterone, whereas progesterone had little effect in the presence of stromal factors from ectopic endometriotic stromal cells. The inability of ectopic endometriotic stromal cells to regulated PI3K/AKt/Survivin signaling and mediate the progesterone response in endometriotic epithelial cells may facilitate epithelial cell proliferation in endometriosis and promote the survival of endometriotic lesions.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometrium Endometrium Epithelial Cells Stromal Cells Adult Blotting, Western Cell Proliferation Cell Proliferation Cells, Cultured Cell Survival Cell Survival Chromones Chromones Endometriosis Endometrium Endometrium Enzyme Inhibitors Enzyme Inhibitors

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 (43)

Cited by (29)

Source provenance

europepmc
last seen: 2026-08-21T06:14:13.963979+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:13:59.677786+00:00
unpaywall
last seen: 2026-08-20T06:30:07.000247+00:00
License: CC0 · commercial use OK