Apoptosis Resistance in Endometriosis

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Endometriotic lesions displayed both apoptotic and proliferative activity in epithelial cells, indicating that persistent tissue requires proliferative cells from lower endometrial layers for survival.

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This study investigated whether programmed cell death is essential for the destruction of dystopic endometrial tissue in endometriosis by examining endometriotic lesions from 15 patients. Using TUNEL staining to measure apoptosis activity and Ki-67 immunostaining to assess epithelial proliferation, the authors found that 12 of 15 women had detectable apoptosis activity (3–47%) alongside epithelial proliferation (2–25%). They concluded that persistence of dystopic endometrium is linked to proliferative epithelial cells in middle to lower endometrial layers, and that misaligned upper-layer epithelium can be eliminated by apoptosis. This paper is centrally about endometriosis — it directly measures apoptosis and proliferation in endometriotic lesions to explain persistence of dystopic tissue.

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Abstract

INTRODUCTION: In a cytological analysis of endometriotic lesions neither granulocytes nor cytotoxic T-cells appear in an appreciable number. Based on this observation we aimed to know, whether programmed cell death plays an essential role in the destruction of dystopic endometrium. Disturbances of the physiological mechanisms of apoptosis, a persistence of endometrial tissue could explain the disease. Another aspect of this consideration is the proliferation competence of the dystopic mucous membrane. METHODS: Endometriotic lesions of 15 patients were examined through a combined measurement of apoptosis activity with the TUNEL technique (terminal deoxyribosyltransferase mediated dUTP Nick End Labeling) and the proliferation activity (with the help of the Ki-67-Antigens using the monoclonal antibody Ki-S5). RESULTS: Twelve out of 15 women studied showed a positive apoptotic activity of 3-47% with a proliferation activity of 2-25% of epithelial cells. Therefore we concluded that the persistence of dystopic endometrium requires proliferative epithelial cells from middle to lower endometrial layers. CONCLUSION: A dystopia misalignment of the epithelia of the upper layers of the functionalism can be rapidly eliminated by apoptotic procedures.
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BioImpacts (Aug 2011) Apoptosis Resistance in Endometriosis Abstract Introduction: In a cytological analysis of endometriotic lesions neither granulocytes nor cytotoxic T-cells appear in an appreciable number. Based on this observation we aimed to know, whether programmed cell death plays an essential role in the destruction of dystopic endometrium. Disturbances of the physiological mechanisms of apoptosis, a persistence of endometrial tissue could explain the disease. Another aspect of this consideration is the proliferation competence of the dystopic mucous membrane. Methods: Endometriotic lesions of 15 patients were examined through a combined measurement of apoptosis activity with the TUNEL technique (terminal deoxyribosyltransferase mediated dUTP Nick End Labeling) and the proliferation activity (with the help of the Ki-67-Antigens using the monoclonal antibody Ki-S5). Results: Twelve out of 15 women studied showed a positive apoptotic activity of 3-47% with a proliferation activity of 2-25% of epithelial cells. Therefore we concluded that the persistence of dystopic endometrium requires proliferative epithelial cells from middle to lower endometrial layers. Conclusion: A dystopia misalignment of the epithelia of the upper layers of the functionalism can be rapidly eliminated by apoptotic procedures.

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endometriosis

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