作者: Jonathan T. McGuane , Katherine M. Watson , Jamie Zhang , M. Zahied Johan , Zhao Wang
DOI: 10.1016/J.AJPATH.2015.01.010
关键词:
摘要: The factors that predispose one-tenth of reproductive-aged women to endometriosis are poorly understood. We determined genetic deficiency in transforming growth factor β1 impairs endometriosis-like lesion mice. Given seminal plasma is an abundant source β, we evaluated the effect exposure on endometrial lesions. Human explants were exposed or control medium before transfer Prkdc(scid)-mutant (severe combined immunodeficient) Xenografts showed eightfold increase volume and a 4.3-fold weight after 14 days. These increases associated with increased proliferation epithelial cells enhanced survival human stromal compared those lesions, which cell persistence was negligible. Although distribution macrophages altered, their number activation status did not change response plasma. Seminal stimulated production variety cytokines tissue, including growth-regulated oncogene, granulocyte macrophage colony-stimulating factor, IL-1β. data suggest enhances formation via direct proliferation, rather than macrophage-mediated mechanisms. findings raise possibility could contribute endometriotic disease progression women.