Blocking of Stromal Cell–Derived Factor-1 Reduces Neoangiogenesis in Human Endometriosis Lesions in a Mouse Model
Version of Record online: 7 MAY 2013
© 2013 John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 70, Issue 5, pages 386–397, November 2013
How to Cite
Blocking of stromal cell–derived factor-1 reduces neoangiogenesis in human endometriosis lesions in a mouse model. Am J Reprod Immunol 2013; 70: 386–397, , , , .
- Issue online: 9 OCT 2013
- Version of Record online: 7 MAY 2013
- Manuscript Accepted: 3 APR 2013
- Manuscript Received: 1 MAR 2013
- Canadian Institutes of Health Research
- Queen's University Principal's development Fund
- endothelial progenitor cell;
- stromal cell–derived factor-1
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.