ROLE OF STROMAL CELL-DERIVED FACTOR-1 IN NEOANGIOGENESIS IN ENDOMETRIOSIS LESIONS

Sophia Virani
2011 · W2182724308
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Stromal cell-derived factor-1 (SDF-1) is abundant in human endometriosis and recruits progenitor cells, and blocking SDF-1 reduced neovascularization of endometriotic lesions in a mouse model.

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This study investigated the role of stromal cell-derived factor-1 (SDF-1) in neoangiogenesis and endothelial progenitor cell (EPC) recruitment in endometriosis lesions by combining analyses of human samples with a murine endometriosis model. The authors performed immunohistochemistry for SDF-1 and CD34 on human endometriosis versus eutopic endometrium, measured SDF-1 and EPCs in peripheral blood by ELISA and flow cytometry, and used BALB/c-Rag2-/-/IL2rg-/- mice treated weekly for four weeks with either an SDF-1 blocking antibody or an isotype control. They found overabundance of SDF-1 and CD34+ progenitor cells in human endometriotic lesions, and in mice lesion vascularity (CD31-positive staining) was reduced in the SDF-1 blocking group compared with controls, consistent with impaired neovascularization. A stated caveat is that the treatment was tested alone and that further studies combining SDF-1 blockade with other antiangiogenic agents are needed. This paper is centrally about endometriosis — it specifically examines how SDF-1 regulates EPC recruitment and neovascularization in endometriosis lesions.

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Role of Stromal Cell-Derived Factor-1 in Neoangiogenesis in Endometriosis Lesions Date Authors Journal Title Journal ISSN Volume Title Publisher Abstract Endometriosis affects 5-10% of women and is characterized by the growth of endometrial tissue outside of the uterus. Treatment for endometriosis primarily focuses on symptom relief, is short term with severe side effects and often leads to recurrence of the condition. Establishing new blood supply is a fundamental requirement for endometriosis lesions growth. This has led to the idea that antiangiogenic therapy may be a successful approach for inhibiting endometriosis. Recent evidence indicates that endothelial progenitor cells (EPCs) contribute to neoangiogenesis of endometriotic lesions. These EPCs are recruited to the lesion site by stromal cell-derived factor-1 (SDF-1). We hypothesize that SDF-1 is central to the neoangiogenesis and survival of endometriotic lesions and that administration of SDF-1 blocking antibody will inhibit lesion growth by inhibiting angiogenesis in a murine model of endometriosis. Immunohistochemistry for SDF-1 and CD34 was performed on human endometriosis and normal endometrial samples. Quantification of SDF-1 and EPCs was performed in the blood of endometriosis patients and controls using ELISA and flow cytometry, respectively. A new mouse model of endometriosis was developed using BALB/c-Rag2-/-/IL2rg-/- mice to investigate role of SDF-1 in neoangiogenesis. Either SDF-1 blocking antibody or an isotype control was administered on a weekly basis for four weeks. Weekly samples of peripheral blood from mice were analyzed for SDF-1, other cytokines of interest and EPCs. Mice were euthanized at seven weeks to observe lesion growth and blood vessel development. Our results indicate overabundance of SDF-1 and CD34+ progenitor cells in human endometriotic lesions compared to eutopic endometrium. In the mouse model, SDF-1 and circulating EPC levels decreased from pre-treatment levels after one week, and remained constant over the course of the treatment in both SDF-1 blocking antibody and isotype control groups. In the SDF-1 blocking group, reduced vascularity of lesions, identified by immunofluorescence staining for CD31, was revealed compared to isotype controls. These findings suggest that SDF-1 may be responsible for CD34+ progenitor cell recruitment to the neoangiogenic sites in endometriosis. Blocking of SDF-1 reduces neovascularization of human endometriotic lesions in a mouse model. Further studies on blocking SDF-1 in combination with other antiangiogenic agents are needed.

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