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Blocking of Stromal Cell–Derived Factor-1 Reduces Neoangiogenesis in Human Endometriosis Lesions in a Mouse Model



Chandrakant Tayade, Department of Biomedical and Molecular Sciences, Queen's University, 18 Stuart Street, Kingston, ON K7L 3N6, Canada.




Endometriosis 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 study

Using 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−/−/IL2rγ−/− 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.


SDF-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.


Blocking SDF-1 reduces neovascularization and survival of lesions in a mouse model of endometriosis.