Influence of the ectopic location on the antigen expression and functional characteristics of endometrioma stromal cells

María José Ruiz-Magaña, Jose Maria Puerta, José M Puerta, Tatiana Llorca, Cristina Méndez-Malagón, Rocío Martínez-Aguilar, Ana Clara Abadía-Molina, Ana Clara Abadía‐Molina, Enrique G Olivares, Carmen Ruiz‐Ruiz, Carmen Ruiz-Ruiz
Reproductive biomedicine online · 2022 · vol. 46(3) , pp. 460–469 · doi:10.1016/j.rbmo.2022.12.005 · PMID:36586747 · W4311255634
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-06 ⓘ

Ectopic endometrioma stromal cells resist decidualization, are resistant to apoptosis, and exhibit reduced migration inhibition compared to eutopic endometrial stromal cells.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

This study compared endometrial stromal cell lines derived from endometriomas (ectopic, eEnSC) and eutopic endometrium from women with endometriosis (eBEnSC) with stromal cells from healthy menstrual blood (mEnSC) and healthy endometrial biopsy (BEnSC) to test whether ectopic-cell alterations are present before ectopic location or acquired there. Using progesterone and cAMP to induce decidualization for up to 28 days, the authors found that some decidual features (morphology change and prolactin expression) occurred similarly in eutopic cell types but not in eEnSC, while CD105 was downregulated in mEnSC, BEnSC, and eBEnSC but not in eEnSC; additionally, mEnSC/BEnSC underwent apoptosis whereas eBEnSC/eEnSC were resistant to apoptosis induction. Migration assays showed that decidualization conditioned mEnSC with factors inhibiting cell motility, whereas eEnSC had a significantly lower ability to produce such migration-regulating factors. This paper is centrally about endometriosis — it directly examines how ectopic location affects antigen expression and functional decidual responses (including apoptosis and migration) in endometrioma-derived stromal cells.

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Abstract

RESEARCH QUESTION: Are the alterations observed in the endometriotic cells, such as progesterone resistance, already present in the eutopic endometrium or acquired in the ectopic location? DESIGN: The response to decidualization with progesterone and cyclic AMP for up to 28 days was compared in different endometrial stromal cell (EnSC) lines established from samples of endometriomas (eEnSC), eutopic endometrium from women with endometriosis (eBEnSC), endometrial tissue from healthy women (BEnSC) and menstrual blood from healthy donors (mEnSC). RESULTS: Usual features of decidualized cells, such as changes in cell morphology and expression of prolactin, were similarly observed in the three types of eutopic EnSC studied, but not in the ectopic cells upon decidualization. Among the phenotypic markers analysed, CD105 was down-regulated under decidualization in all cell types (mEnSC, P = 0.005; BEnSC, P = 0.029; eBEnSC, P = 0.022) except eEnSC. mEnSC and BEnSC underwent apoptosis during decidualization, whereas eBEnSC and eEnSC were resistant to the induction of cell death. Lastly, migration studies revealed that mEnSC secreted undetermined factors during decidualization that inhibited cell motility, whereas eEnSC showed a significantly lower ability to produce those migration-regulating factors (P < 0.0001, P  < 0.001 and P = 0.0013 for the migration of mEnSC at 24, 48 and 72 h, respectively; P  < 0.0001 for the migration of eEnSC at all times studied). CONCLUSIONS: This study provides novel insights into the differences between endometriotic and eutopic endometrial cells and reinforces the idea that the microenvironment in the ectopic location plays additional roles in the acquisition of the alterations that characterize the cells of the endometriotic foci.

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Condition tags

endometriosisendometrioma

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Uterine Diseases Uterine Diseases Uterine Diseases Uterine Diseases

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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.

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