Pregnancy affects morphology of induced endometriotic lesions in a mouse model through alteration of proliferation and angiogenesis

J. Cohen, Jonathan Cohen, Cohen J, Iptissem Naoura, Naoura I, I. Naoura, M Castela, Mathieu Castela, Von N'Guyen T, Tuan Nguyen, T Von N'Guyen, M. Oster, Oster M, R Fontaine, Fontaine R, Nathalie Chabbert‐Buffet, Chabbert-Buffet N, N Chabbert-Buffet, Émile Daraï, Darai E, E Darai, S. Aractingi
European journal of obstetrics, gynecology, and reproductive biology · 2014 · vol. 183 , pp. 70–77 · doi:10.1016/j.ejogrb.2014.10.038 · PMID:25461356 · W1999678075
Lab / animal OA: closed CC0 ⤵ 5 in-corpus citations
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This study investigated how pregnancy influences induced endometriotic lesions in mice by examining changes in lesion morphology, specifically focusing on proliferation and angiogenesis.

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Abstract

OBJECTIVE: Pregnancy is known to alleviate the symptoms of endometriosis and is also known to be a pro-angiogenic condition affecting blood and lymphatic vessels. However, angiogenesis actively participates in the development of endometriosis. The objective of our study was to study the impact of pregnancy on endometriotic tissue. Study design We performed a cross-sectional, control versus treatment study in a mouse model of endometriosis. Thirty-one female C57Bl6 mice were mated and became pregnant and 31 females were not mated and served as control. Intraperitoneal endometriotic lesions were surgically induced in C57Bl6 mice which were subsequently mated or not (group P: pregnant, group NP: non-pregnant). P and NP mice were sacrificed on day E15.5 of the pregnancy of P mice and lesions were harvested. Lesions were weighed and analyzed by histology, immunohistology, flow cytometry and real-time quantitative RT-PCR (qRT-PCR). RESULTS: Pregnancy reduced lesion weight, decreased the proportion of cystic component (0.02 vs. 0.4; p<0.001) and modified the architecture of peritoneal endometriotic lesions. Pregnancy also increased cell proliferation in both stromal and glandular tissue as shown by the increase in Ki 67-positive cells in the P group (glandular: 19 vs. 3.9%, p<0.001; stromal: 8.7 vs. 3.3%, p<0.01). Finally, pregnancy increased angiogenesis in endometriotic lesions as indicated by an increased microvessel density (CD-31 and LYVE-1 stainings: respectively 2.2 vs. 5.1%, p<0.01 and 0.4 vs. 0.9%, p<0.001), an increased number of LYVE1 positive cells evaluated by flow cytometry (18.9 vs. 4.6%, p<0.05) and a rise in VEGF-A, -R2 and -R3 RNA expression shown by qRT-PCR (p<0.001; p<0.01; p<0.05). CONCLUSION: These challenging results provide insight in understanding the pathophysiology of endometriosis and evoke a correlation between lesion architecture and symptomatology.

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Condition tags

endometriosis

MeSH descriptors

Cell Proliferation Endometriosis Endometriosis Endometrium Neovascularization, Pathologic Pregnancy, Animal Animals Animals Cell Proliferation Cell Proliferation Cross-Sectional Studies Cross-Sectional Studies Disease Models, Animal Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (65)

Cited by (6)

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