Suppression of matrix metalloproteinases inhibits establishment of ectopic lesions by human endometrium in nude mice.

K L Bruner, Lynn M. Matrisian, L M Matrisian, William H. Rodgers, W H Rodgers, Fred Gorstein, F Gorstein, Kevin G. Osteen, K G Osteen
The Journal of clinical investigation · 1997 · vol. 99(12) , pp. 2851–2857 · doi:10.1172/jci119478 · PMID:9185507 · PMC508135 · W2105925637
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

In a mouse model, estrogen increased matrix metalloproteinase secretion from human endometrium, promoting ectopic lesion formation, while progesterone or a metalloproteinase inhibitor suppressed lesion establishment.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This paper studied whether matrix metalloproteinases (stromelysin family) in human endometrium contribute to the establishment of ectopic endometrial lesions, using an athymic nude mouse model in which human endometrial tissue was injected to form peritoneal lesions. The authors found that estrogen treatment in organ culture maintained matrix metalloproteinase secretion and promoted lesion establishment, whereas progesterone-induced suppression of metalloproteinase secretion or pharmacologic inhibition of enzyme activity reduced ectopic lesion formation. A key caveat is that the work uses a mouse recipient model with human tissue rather than directly measuring endometriosis development in humans. This paper is centrally about endometriosis — it experimentally tests how endometrial matrix metalloproteinase secretion and inhibition affect the formation of ectopic peritoneal lesions.

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Abstract

Matrix metalloproteinases of the stromelysin family are expressed in the human endometrium as a consequence of cellular events during the menstrual cycle that require extracellular matrix remodeling. We have recently documented the presence of these enzymes in lesions of endometriosis, a benign disease that presents as persistent ectopic sites of endometrial tissue, usually within the peritoneal cavity. Endometriosis can develop after retrograde menstruation of endometrial tissue fragments, and establishment of ectopic sites within the peritoneal cavity requires breakdown of extracellular matrix. To examine whether matrix metalloproteinases might contribute to the steroid-dependent epidemiology and cellular pathophysiology of endometriosis, we have developed an experimental model of endometriosis using athymic nude mice as recipients of human endometrial tissue. Our results demonstrate that estrogen treatment of human endometrial tissue in organ culture maintains secretion of matrix metalloproteinases, and promotes establishment of ectopic peritoneal lesions when injected into recipient animals. In contrast, suppressing metalloproteinase secretion in vitro with progesterone treatment, or blocking enzyme activity with a natural inhibitor of metalloproteinases, inhibits the formation of ectopic lesions in this experimental model.
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Advertisement Research Article Free access | 10.1172/JCI119478 Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. Find articles by Bruner, K. in: PubMed | Google Scholar Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. Find articles by Matrisian, L. in: PubMed | Google Scholar Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. Find articles by Rodgers, W. in: PubMed | Google Scholar Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. Find articles by Gorstein, F. in: PubMed | Google Scholar Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA. Find articles by Osteen, K. in: PubMed | Google Scholar Published June 15, 1997 - More info Published in Volume 99, Issue 12 on June 15, 1997 J Clin Invest. 1997;99(12):2851–2857. https://doi.org/10.1172/JCI119478. © 1997 The American Society for Clinical Investigation J Clin Invest. 1997;99(12):2851–2857. https://doi.org/10.1172/JCI119478. © 1997 The American Society for Clinical Investigation Published June 15, 1997 - Version history - Abstract Matrix metalloproteinases of the stromelysin family are expressed in the human endometrium as a consequence of cellular events during the menstrual cycle that require extracellular matrix remodeling. We have recently documented the presence of these enzymes in lesions of endometriosis, a benign disease that presents as persistent ectopic sites of endometrial tissue, usually within the peritoneal cavity. Endometriosis can develop after retrograde menstruation of endometrial tissue fragments, and establishment of ectopic sites within the peritoneal cavity requires breakdown of extracellular matrix. To examine whether matrix metalloproteinases might contribute to the steroid-dependent epidemiology and cellular pathophysiology of endometriosis, we have developed an experimental model of endometriosis using athymic nude mice as recipients of human endometrial tissue. Our results demonstrate that estrogen treatment of human endometrial tissue in organ culture maintains secretion of matrix metalloproteinases, and promotes establishment of ectopic peritoneal lesions when injected into recipient animals. In contrast, suppressing metalloproteinase secretion in vitro with progesterone treatment, or blocking enzyme activity with a natural inhibitor of metalloproteinases, inhibits the formation of ectopic lesions in this experimental model. - Version history - Version 1 (June 15, 1997): No description Advertisement Advertisement Copyright © 2026 American Society for Clinical Investigation ISSN: 0021-9738 (print), 1558-8238 (online)

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Metalloendopeptidases Protease Inhibitors Adult Animals Disease Models, Animal Endometriosis Endometrium Endometrium Estradiol Estradiol Female Glycoproteins Glycoproteins Humans Metalloendopeptidases Metalloendopeptidases Mice Mice, Nude

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