Estrogen is essential but not sufficient to induce endometriosis
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Endometriosis is a common gynaecological disorder of unknown aetiology. Among the several factors, estrogen has been implicated as a causative factor in endometriosis. In the present study using mouse model, we assessed the role of estrogen in the initial implantation and growth of endometrium in ectopic locations. Uterine tissues from green fluorescent protein (GFP) mice were transplanted in to the peritoneum of wild type mice in presence and absence of estrogen. As compared to untreated controls, the implantation of uterine tissue at ectopic locations was higher when estrogen was administered to both host and donor animals. However, this effect was not sustained as lesions regressed within 14 days of treatment. Irrespective of the treatment, peritoneal adipose was the most preferred site of lesion establishment. The lesions did not have typical features of the endometriosis (presence of glands and stroma) even after estrogen treatment and the ectopic tissue underwent regression by apoptosis irrespective of treatment. Since estrogen promotes implantation of endometrial tissue to ectopic locations but failure of these ectopic lesions to grow and sustain even in high estrogenic environment we propose that estrogen is necessary but not sufficient to sustain endometriosis.
KeywordsApoptosis endometriosis estrogen GFP mice transplantation
We express our gratitude to the staff of Experimental Animal Facility for providing the animals in timely manner. The help extended by Mr. Suryakant (NEC division, NIRRH) towards histological preparations is gratefully acknowledged. The study was financially supported by grants from Department of Biotechnology (BT/PR6587/MED/30/886/2010) to DM and intramural support from the Indian Council of Medical Research (ICMR), New Delhi. MG is a recipient of the ICMR- postdoctoral fellowship (6th batch). NS is financially supported by a JRF from a DBT project (BT/514/NE/TBP/2013) to DM.
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