Leukocyte driven-decidual angiogenesis in early pregnancy

Abstract

Successful pregnancy and long-term, post-natal maternal and offspring cardiac, vascular and metabolic health require key maternal cardiovascular adaptations over gestation. Within the pregnant decidualizing uterus, coordinated vascular, immunological and stromal cell changes occur. Considerable attention has been given to the roles of uterine natural killer (uNK) cells in initiating decidual spiral arterial remodeling, a process normally completed by mid-gestation in mice and in humans. However, leukocyte roles in much earlier, region specific, decidual vascular remodeling are now being defined. Interest in immune cell-promoted vascular remodeling is driven by vascular aberrations that are reported in human gestational complications such as infertility, recurrent spontaneous abortion, preeclampsia (PE) and fetal growth restriction. Appropriate maternal cardiovascular responses during pregnancy protect mothers and their children from later cardiovascular disease risk elevation. One of the earliest uterine responses to pregnancy in species with hemochorial placentation is stromal cell decidualization, which creates unique niches for angiogenesis and leukocyte recruitment. In early decidua basalis, the aspect of the implantation site that will cradle the developing placenta and provide the major blood vessels to support mature placental functions, leukocytes are greatly enriched and display specialized properties. UNK cells, the most abundant leukocyte subset in early decidua basalis, have angiogenic abilities and are essential for normal early decidual angiogenesis. The regulation of uNK cells and their roles in determining maternal and progeny cardiovascular health over pregnancy and postpartum are discussed.

Therapeutic effects of Wharton jelly‐derived mesenchymal stem cells on rat abortion models

“…3,4 Imbalance of Th1 and Th2 cytokine production of peripheral lymphocytes were found in RPL women. Th1 cells secreted various cytokines, including IL-2 and IFN-γ, which mediated cellular immunity.…”

“…However, abnormality of the maternal immune system may induce pre-eclampsia and RPL. 3,4 These factors include various humoral abnormalities as well as cellular components, which may be associated with toxicity to the trophoblast, placenta or fetus, leading to RPL. The imbalance of Th1 and Th2 cytokine production of peripheral lymphocytes has been found in URSA.…”

Are There Any Differences Between the Distribution of Placental Bed Leukocyte Subtypes and Plasma Cytokine Levels of Preeclamptic and Healthy Pregnants?

“…Dysregulation of the interaction among macrophage, NK and T-cells may lead to PE [31][32][33]. According to study of Lockwood et al excess macrophage-derived TNF-a production interferes with normal stepwise spiral artery remodelling and leading to PE.…”

Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface

“…On the maternal side of the interface, the decidua recruits a heterogeneous pool of leukocytes that in mice account for 30% to 50% of all decidual cells. In addition to their participation in maternal immune tolerance, these cells are key contributors to different processes during pregnancy, e.g., the protection of the reproductive tract from infections, fecundation, embryo implantation 7,25 , decidual angiogenesis 26 , vascular remodeling 24,27 , trophoblast invasion 28 , placental development 24,25 . Flow cytometric analysis of leukocytes at the maternal-fetal interface requires a singlecell suspension.…”