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Research Article Free access | 10.1172/JCI119478

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

K L Bruner, L M Matrisian, W H Rodgers, F Gorstein, and K G Osteen

Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Bruner, K. in: JCI | PubMed | Google Scholar

Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Matrisian, L. in: JCI | PubMed | Google Scholar

Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Find articles by Rodgers, W. in: JCI | PubMed | Google Scholar

Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

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Department of Obstetrics and Gynecology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

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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
Published June 15, 1997 - Version history
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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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