Estrogen is essential but not sufficient to induce endometriosis

Mosami Galvankar, Neha Singh, Deepak Modi
Journal of biosciences · 2017 · vol. 42(2) , pp. 251–263 · doi:10.1007/s12038-017-9687-4 · PMID:28569249 · W2612041521
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-12 ⓘ

In a mouse model, estrogen administration increased initial ectopic endometrial implantation, but lesions regressed within 14 days, indicating estrogen is necessary but not sufficient for endometriosis.

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The study investigated whether estrogen is sufficient to induce and sustain endometriosis-like lesions by using a mouse model in which GFP-labeled uterine tissue was transplanted into the peritoneum of wild-type recipient mice with or without administered estrogen to both host and donor. Uterine tissue implantation at ectopic locations increased with estrogen exposure, but the resulting lesions regressed within 14 days of treatment and did not develop typical endometriosis histologic features such as glands and stroma. Regression occurred via apoptosis regardless of estrogen treatment, leading the authors to conclude that estrogen is necessary for ectopic implantation but not sufficient for lesion growth and maintenance. This paper is centrally about endometriosis — it specifically tests estrogen’s role in initial implantation and subsequent growth/regression of ectopic uterine tissue in a mouse model.

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Abstract

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. Similar content being viewed by others

References

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Acknowledgements

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. Author information Authors and Affiliations Corresponding author Additional information Corresponding editor: S Shivaji Rights and permissions About this article Cite this article Galvankar, M., Singh, N. & Modi, D. Estrogen is essential but not sufficient to induce endometriosis. J Biosci 42, 251–263 (2017). https://doi.org/10.1007/s12038-017-9687-4 Received: Accepted: Published: Issue date: DOI: https://doi.org/10.1007/s12038-017-9687-4

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endometriosis

MeSH descriptors

Endometriosis Estrogens Animals Choristoma Endometriosis Endometrium Endometrium Estrogens Female Gene Expression Regulation Mice Mice, Inbred C57BL Receptors, Estrogen Receptors, Estrogen Receptors, Estrogen Tissue Transplantation

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