Results
| PMID | 23650939 |
| Gene Name | CD34 |
| Condition | Endometriosis |
| Association |
Associated |
| Sex | Female |
| Other associated phenotypes |
Endometriosis |
|
Am J Reprod Immunol. 2013 Nov;70(5):386-97. doi: 10.1111/aji.12134. Epub 2013 May Virani, Sophia| Edwards, Andrew K| Thomas, Richard| Childs, Timothy| Tayade, Chandrakant Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada. 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(-/-) /IL2rgamma(-/-) 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. Mesh Terms: Animals| Antibodies, Blocking/administration & dosage| Antigens, CD34/metabolism| Chemokine CXCL12/immunology/*metabolism| Disease Models, Animal| Endometriosis/immunology/pathology/*therapy| Endometrium/pathology/transplantation| Endothelium, Vasc |
|