Journal
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
Volume 70, Issue 5, Pages 386-397Publisher
WILEY-BLACKWELL
DOI: 10.1111/aji.12134
Keywords
Angiogenesis; endometriosis; endothelial progenitor cell; stromal cell-derived factor-1
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Funding
- Canadian Institutes of Health Research
- Queen's University Principal's Development Fund
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ProblemEndometriosis affects 5-10% of women and is characterized by the growth of endometrial tissue outside of the uterus. Establishing new blood supply is a fundamental requirement for endometriosis lesion growth. Endothelial progenitor cells (EPCs), recruited by stromal cell-derived factor-1 (SDF-1), contribute to neoangiogenesis in endometriotic lesions. We hypothesized that SDF-1 is central to the neoangiogenesis and survival of endometriotic lesions, and blocking of SDF-1 will reduce vascularization of lesions in a mouse model. Method of studyUsing immunohistochemistry, we evaluated SDF-1 and CD34(+) EPCs in human endometriotic lesions and normal endometrium samples. EPCs were co-localized using CD34 and VEGFR2. Effects of SDF-1 blocking on endometriotic lesion survival were assessed in BALB/c-Rag2(-/-)/IL2r(-/-) mice engrafted with human endometrium and treated with SDF-1-blocking antibody or an isotype control. Weekly blood samples from experimental mice were analyzed for cytokines and EPCs. ResultsSDF-1 and CD34(+) EPCs were abundant in human endometriotic lesions compared with eutopic endometrium. In our mouse model, SDF-1-blocking antibody reduced CD31(+) microvessels compared with isotype control. ConclusionBlocking SDF-1 reduces neovascularization and survival of lesions in a mouse model of endometriosis.
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