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

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Blocking stromal cell-derived factor-1 (SDF-1) reduced neovascularization and lesion survival in a mouse model of human endometriosis by decreasing endothelial progenitor cell recruitment.

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Abstract

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

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Chemokine CXCL12 Endometriosis Endothelium, Vascular Microvessels Neovascularization, Pathologic Animals Antibodies, Blocking Antibodies, Blocking Antigens, CD34 Antigens, CD34 Chemokine CXCL12 Chemokine CXCL12 Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Endothelium, Vascular

Citation neighborhood

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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (49)

Cited by (19)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
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pubmed
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