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A novel mouse model of endometriosis mimics human phenotype and reveals insights into the inflammatory contribution of shed endometrium

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Greaves, Erin, Cousins, Fiona L., Murray, Alison, Esnal-Zufiaurre, Arantza, Fassbender, Amelie, Horne, Andrew W. and Saunders, Philippa T.K. (2014) A novel mouse model of endometriosis mimics human phenotype and reveals insights into the inflammatory contribution of shed endometrium. The American Journal of Pathology, 184 (7). pp. 1930-1939. doi:10.1016/j.ajpath.2014.03.011 ISSN 00029440.

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Official URL: http://dx.doi.org/10.1016/j.ajpath.2014.03.011

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Abstract

Endometriosis is an estrogen-dependent inflammatory disorder characterized by the presence of endometrial tissue outside the uterine cavity. Patients experience chronic pelvic pain and infertility, with the most likely origin of the tissue deposits (lesions) being endometrial fragments shed at menses. Menstruation is an inflammatory process associated with a dramatic increase in inflammatory mediators and tissue-resident immune cells. In the present study, we developed and validated a mouse model of endometriosis using syngeneic menstrual endometrial tissue introduced into the peritoneum of immunocompetent mice. We demonstrate the establishment of endometriotic lesions that exhibit similarities to those recovered from patients undergoing laparoscopy. Specifically, in both cases, lesions had epithelial (cytokeratin(+)) and stromal (vimentin/CD10(+)) cell compartments with a well-developed vasculature (CD31(+) endothelial cells). Expression of estrogen receptor β was increased in lesions compared with the peritoneum or eutopic endometrium. By performing experiments using mice with green fluorescent protein-labeled macrophages (MacGreen) in reciprocal transfers with wild-type mice, we obtained evidence that macrophages present in the peritoneum and in menses endometrium can contribute to the inflammatory microenvironment of the lesions. In summary, we developed a mouse model of endometriosis that exhibits similarities to human peritoneal lesions with respect to estrogen receptor expression, inflammation, and macrophage infiltration, providing an opportunity for further studies and the possible identification of novel therapies for this perplexing disorder.

Item Type: Journal Article
Divisions: Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Cell & Developmental Biology
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences
Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School
Journal or Publication Title: The American Journal of Pathology
Publisher: Elsevier
ISSN: 00029440
Official Date: 4 June 2014
Dates:
DateEvent
4 June 2014Published
20 March 2014Accepted
Volume: 184
Number: 7
Page Range: pp. 1930-1939
DOI: 10.1016/j.ajpath.2014.03.011
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access
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