Effects of anti-endometriotic therapies on Fas-mediated endometrial epithelial apoptosis

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Endometriotic and healthy women's sera inhibited Fas-mediated endometrial epithelial cell apoptosis, suggesting eutopic apoptosis reduction stems from stromal cell effects rather than direct serum epithelial interactions.

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The study assessed how sera from seven endometriotic patients, compared with sera from healthy women, affect proliferation and Fas-mediated apoptosis in the human endometrial epithelial cell line HHUA, using cell-based assays and focusing on epithelial apoptosis with functional hormone receptors. The key finding was that cell proliferation was unchanged by any sera, but sera from six of seven endometriotic patients (and two healthy women) significantly inhibited Fas-mediated apoptosis. Anti-apoptotic activity in endometriotic sera was not altered after gonadotropin-releasing hormone agonist therapy for four weeks or Keishi-bukuryo-gan therapy for twelve weeks, and the authors propose that reduced eutopic epithelial apoptosis in endometriosis may reflect secondary effects from stromal growth and circulating surviving factors rather than direct epithelial effects. This paper is centrally about endometriosis — it tests how anti-endometriotic therapies and patient sera influence Fas-mediated apoptosis in endometrial epithelial cells.

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Abstract

Decreased numbers of eutopic endometrial apoptotic cells have been reported in endometriotic patients, indicating the possibility of anti-apoptotic effects of their sera. Recently, we reported that the sera from endometriotic patients enhance endometrial stromal cell proliferation and viability, and that Keishi-bukuryo-gan therapy, an anti-endometriotic Japanese herbal medicine, reduces anti-apoptotic activities in the sera. In this study, we therefore examined the effects of sera from 7 endometriotic patients on cell proliferation and Fas-mediated apoptosis of the human endometrial epithelial cell line HHUA, which has a normal karyotype and functional estrogen and progesterone receptors. Cell proliferation was not affected by any of the sera examined, including sera from healthy women. The sera of 6 out of 7 endometriotic patients and sera from 2 healthy women significantly inhibited Fas-mediated apoptosis in the cells. Moreover, anti-apoptotic activities in the sera of endometriotic patients on Fas-mediated apoptosis were not affected by gonadotropin-releasing hormone agonist (GnRHa) therapy within 4 weeks or Keishi-bukuryo-gan therapy within 12 weeks. Considering these results, we suggest that the surviving factor(s) against Fas-mediated endometrial epithelial cell apoptosis in human sera can be found in endometriotic and non-endometriotic women, and that decreased eutopic endometrial epithelial apoptosis in endometriotic patients might be caused by the secondary effects of endometrial stromal cell growth and surviving factor(s) in sera of the patients, not by direct serum effects on the epithelium.
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Print ISSN: 1021-335X Online ISSN: 1791-2431 International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease. International Journal of Oncology is an international journal devoted to oncology research and cancer treatment. Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery. Oncology Reports is an international journal devoted to fundamental and applied research in Oncology. Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine. Oncology Letters is an international journal devoted to Experimental and Clinical Oncology. Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology. International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis. Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology. Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition. Publishes open-access research on using epigenetics to advance understanding and treatment of human disease. An International Open Access Journal Devoted to General Medicine. Article - Authors: - Pages: 1235-1239|Published online on: June 1, 2005https://doi.org/10.3892/or.13.6.1235 - Expand metrics + Decreased numbers of eutopic endometrial apoptotic cells have been reported in endometriotic patients, indicating the possibility of anti-apoptotic effects of their sera. Recently, we reported that the sera from endometriotic patients enhance endometrial stromal cell proliferation and viability, and that Keishi-bukuryo-gan therapy, an anti-endometriotic Japanese herbal medicine, reduces anti-apoptotic activities in the sera. In this study, we therefore examined the effects of sera from 7 endometriotic patients on cell proliferation and Fas-mediated apoptosis of the human endometrial epithelial cell line HHUA, which has a normal karyotype and functional estrogen and progesterone receptors. Cell proliferation was not affected by any of the sera examined, including sera from healthy women. The sera of 6 out of 7 endometriotic patients and sera from 2 healthy women significantly inhibited Fas-mediated apoptosis in the cells. Moreover, anti-apoptotic activities in the sera of endometriotic patients on Fas-mediated apoptosis were not affected by gonadotropin-releasing hormone agonist (GnRHa) therapy within 4 weeks or Keishi-bukuryo-gan therapy within 12 weeks. Considering these results, we suggest that the surviving factor(s) against Fas-mediated endometrial epithelial cell apoptosis in human sera can be found in endometriotic and non-endometriotic women, and that decreased eutopic endometrial epithelial apoptosis in endometriotic patients might be caused by the secondary effects of endometrial stromal cell growth and surviving factor(s) in sera of the patients, not by direct serum effects on the epithelium. Copy and paste a formatted citation Spandidos Publications style Tanaka T: Effects of anti-endometriotic therapies on Fas-mediated endometrial epithelial apoptosis. Oncol Rep 13: 1235-1239, 2005. APA Tanaka, T. (2005). Effects of anti-endometriotic therapies on Fas-mediated endometrial epithelial apoptosis. Oncology Reports, 13, 1235-1239. https://doi.org/10.3892/or.13.6.1235 MLA Tanaka, T."Effects of anti-endometriotic therapies on Fas-mediated endometrial epithelial apoptosis". Oncology Reports 13.6 (2005): 1235-1239. Chicago Tanaka, T."Effects of anti-endometriotic therapies on Fas-mediated endometrial epithelial apoptosis". Oncology Reports 13, no. 6 (2005): 1235-1239. https://doi.org/10.3892/or.13.6.1235

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Autoantibodies Cell Proliferation Drugs, Chinese Herbal Endometriosis Endometrium Epithelial Cells fas Receptor Adult Autoantibodies Autoantibodies Cell Proliferation Drugs, Chinese Herbal Endometriosis Endometrium Endometrium Endometrium Epithelial Cells Epithelial Cells Epithelial Cells

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