Müllerian Inhibiting Substance Induces Apoptosis of Human Endometrial Stromal Cells in Endometriosis

Jeong Namkung, Jae Yen Song, Hyun Hee Jo, Mee Ran Kim, Mee‐Ran Kim, Young Oak Lew, Patricia K Donahoe, David T MacLaughlin, Jang Heub Kim
The Journal of clinical endocrinology and metabolism · 2012 · vol. 97(9) , pp. 3224–3230 · doi:10.1210/jc.2012-1538 · PMID:22761458 · PMC6287505 · W2127674377
article OA: bronze CC0 ⤵ 11 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Müllerian inhibiting substance (MIS) receptor II is expressed in human endometrial stromal cells (ESC) from endometriosis patients, and MIS treatment inhibits ESC proliferation and induces apoptosis in vitro.

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Abstract

CONTEXT: Müllerian inhibiting substance (MIS) is produced in Sertoli cells of fetal testis and causes regression of müllerian ducts in male embryos. MIS also can induce the cell cycle arrest and apoptosis in müllerian duct-derived tumors in vivo and in vitro. OBJECTIVE: Our objective was to investigate the expression of MIS type II receptor (MISR II) and whether MIS can inhibit the proliferation and induce apoptosis in primary cultures of endometrial stromal cells (ESC) of endometriosis. DESIGN AND SETTINGS: In vitro experiments were performed in the university research laboratory. PARTICIPANTS: Tissue samples from 12 patients who had undergone evisceration for ovarian endometrial cysts were included in this study. INTERVENTIONS AND MAIN OUTCOME MEASURES: The expression of MISR II in ESC was investigated by immunohistochemistry. The cell viability and apoptosis in ESC treated with MIS was measured by methylthiazoletetrazolium assay and annexin V analysis. The expression of regulatory proteins in ESC treated with MIS was shown by Western blotting. RESULTS: ESC showed specific immunostaining for the MISR II. ESC treated with MIS exhibited 32% growth inhibition (P = 0.0001). The changes in cell cycle distribution after MIS exposure at 72 h demonstrated that S and G(2)M phases were decreased; G(0)G(1) and sub-G(0)G(1) phases were increased. ESC treated with MIS showed 13.72% annexin V-fluorescein isothiocyanate positivity. In the ESCs, which contain defective p16, MIS increased the expression of pocket proteins p107 and p130 and decreased E2F transcription factor 1. CONCLUSIONS: The results support a central role for MIS in endometriosis. Although the precise mechanism of MIS-mediated inhibition of ESC growth has not been fully defined, these data suggest that MIS has activity against ESC in vitro and may also be an effective targeted therapy for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Anti-Mullerian Hormone Apoptosis Endometriosis Endometrium Stromal Cells Annexin A5 Annexin A5 Annexin A5 Anti-Mullerian Hormone Apoptosis Blotting, Western Cell Cycle Cell Cycle Cell Line, Tumor Cells, Cultured E2F Transcription Factors E2F Transcription Factors Endometriosis Endometriosis Endometrium

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