期刊
JOURNAL OF REPRODUCTION AND DEVELOPMENT
卷 53, 期 3, 页码 455-463出版社
SOCIETY REPRODUCTION & DEVELOPMENT-SRD
DOI: 10.1262/jrd.18170
关键词
angiogenesis; fetal loss; pro-inflammatory cytokines; uterine natural killer cells
Meat pig breeds used commercially in North America lose significant numbers of genetically-normal fetuses in the peri-implantation (attachment) period and at mid-gestation (day 50 of the 114 day gestation interval). Fetal demand that is in excess to the placental blood supply is thought to underlie these waves of fetal loss. In many species, the endometrium of early normal pregnancy is enriched in innate immune cells, particularly uterine natural killer (uNK) cells. In pigs, a species with epitheliochorial placentation, conceptuses mediate about a three-fold enrichment in uNK cells at attachment sites but the functions of these cells are unknown. In species with hemochorial placentation, uNK cells are highly enriched during the process of decidualization and promote endometrial angiogenesis. We have conducted molecular analyses using pure samples of endometrial lymphocytes or endothelium and trophoblast from healthy and arresting conceptus attachment sites in Yorkshire gilts immediately post-attachment [gestation day (GD) 20] and at mid pregnancy (GD50). In healthy sites, angiogenesis was more robustly promoted by lymphocytes than by trophoblasts. An early sign of impending fetal arrest was loss of vascular endothelial growth factor (VEGF) transcription from the lymphocytes and elevation in transcription of the pro-inflammatory gene Interferon (IFN)-gamma. We have postulated that newly differentiated endometrial endothelial cells, not fetal trophoblasts, are damaged by the maternal withdrawal of vascular support and onset of inflammation and that this endometrial damage contributes significantly to peri-implantation fetal death.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据