Uterine natural killer cells as modulators of the maternal-fetal vasculature

Matson, Brooke C.; Caron, Kathleen M.

doi:10.1387/ijdb.140032kc

Cited by 20 publications

(14 citation statements)

References 61 publications

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“…CD34 is a transmembrane protein expressed in hematopoietic progenitor cells, vascular endothelial cells, and embryonic fibroblasts (Wood et al, 1997). Restraint stress decreases the density of uterine natural killer (uNK) cells in the endometrium (Liu et al, 2014), and uNK cells directly or indirectly contribute to the critical process of maternal (Matson & Caron, 2014). Hence, the present study investigated whether the negative effect of restraint stress is exerted via impaired development of endometrial blood vessesl during embryo implantation.…”

Section: Introductionmentioning

confidence: 95%

Restraint stress delays endometrial adaptive remodeling during mouse embryo implantation

Liu¹,

Dong²,

Wang³

et al. 2015

Stress

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We showed previously in mice that restraint stress reduces the number of embryo implantation sites in the endometrium. Here we hypothesized that the uterine microenvironment is altered by restraint stress and consequently is sub-optimal for embryo implantation. On embryonic day 1 (E1), 60 of 154 pregnant CD1 mice underwent restraint stress (4h), repeated daily to E3, E5 or E7 (n = 10 mice per group). Restraint stress decreased food intake and suppressed body weight gain on E3, E5 and E7. Restraint stress decreased the actual and relative weight (percent body weight) of uterus and ovary on E5 (by 14.9%, P = 0.03; 16.1%, P = 0.004) and E7 (by 16.8%, P = 0.03; 20.0%, P = 0.01). Morphologically, restraint stress decreased relative endometrial area (by 8.94-18.8%, P = 0.003-0.021) and uterine gland area (by 30.6%, P < 0.01 on E3 and 44.5%, P < 0.01 on E5). Immunohistochemistry showed that restraint stress decreased microvessel density (by 12.9-70.5%, P < 0.01) and vascular endothelial growth factor expression (by 14.6-45.9%, P = 0.007-0.02). Restraint stress decreased by 32.4-39.8% (P = 0.002-0.01) the mean optical density ratio for proliferating cell nuclear antigen/terminal deoxynucleotidyl transferase dUTP nick end labeling. Methyl thiazolyl tetrazolium assay showed a dosedependent decrease in proliferative activity of endometrial stromal cells (from 52 of 154 pregnant E5 control mice) incubated with H 2 O 2 (100-1000 μM) in vitro. These findings supported the hypothesis that restraint stress negatively influences endometrial adaptive remodeling via an oxidative stress pathway, which resulted in fewer implantation sites. Stress Downloaded from informahealthcare.com by Nanyang Technological University on 08/26/15 For personal use only. Stress Downloaded from informahealthcare.com by Nanyang Technological University on 08/26/15 For personal use only. Stress Downloaded from informahealthcare.com by Nanyang Technological University on 08/26/15 For personal use only. Stress Downloaded from informahealthcare.com by Nanyang Technological University on 08/26/15 For personal use only. Stress Downloaded from informahealthcare.com by Nanyang Technological University on 08/26/15 For personal use only.

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Section: Introductionmentioning

confidence: 95%

Restraint stress delays endometrial adaptive remodeling during mouse embryo implantation

Liu¹,

Dong²,

Wang³

et al. 2015

Stress

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“…The arteries also lose their smooth muscle and become greatly dilated, a process known as spiral artery remodeling (Adamson et al, 2002). Cell ablation experiments have shown that SpA-TGCs are critical to initiate the remodeling (Hu and Cross, 2011), though the remodeling occurs well upstream of even the deepest invading SpA-TGCs (Adamson et al, 2002), and is thought to involve interactions with maternal uterine NK cells (Matson and Caron, 2014;Soares et al, 2014). The spiral arteries converge to form a large canal that carries oxygenated blood to the base of the placenta where it then enters the small sinusoid spaces within the labyrinth spaces lined by canal TGCs (C-TGC) and sinusoidal TGCs (S-TGC), respectively.…”

Section: Introductionmentioning

confidence: 99%

Three-dimensional cultures of trophoblast stem cells autonomously develop vascular-like spaces lined by trophoblast giant cells

Rai

Cross

2015

Developmental Biology

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The maternal blood space in the mouse placenta is lined not by endothelial cells but rather by various subtypes of trophoblast giant cells (TGCs), defined by their location and different patterns of gene expression. While TGCs invade the spiral arteries to displace the maternal endothelium, the rest of the vascular space is created de novo but the mechanisms are not well understood. We cultured mouse trophoblast stem (TS) cells in suspension and found that they readily form spheroids (trophospheres). Compared to cells grown in monolayer, differentiating trophospheres showed accelerated expression of TGC-specific genes. Morphological and gene expression studies showed that cavities form within the trophospheres that are primarily lined by Prl3d1/Pl1α-positive cells analogous to parietal-TGCs (P-TGCs) which line the maternal venous blood within the placenta. Lumen formation in trophospheres and in vivo was associated with cell polarization including CD34 sialomucin deposition on the apical side and cytoskeletal rearrangement. While P-TGCs preferentially formed in trophospheres at atmospheric oxygen levels (19%), decreasing oxygen to 3% shifted differentiation towards Ctsq-positive sinusoidal and/or channel TGCs. These studies show that trophoblast cells have the intrinsic ability to form vascular channels in ways analogous to endothelial cells. The trophosphere system will be valuable for assessing mechanisms that regulate specification of different TGC subtypes and their morphogenesis into vascular spaces.

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“…Remodeling of uterine spiral arteries, conduits of the uteroplacental circulation, is critical for proper placentation [5] and is accomplished in part by crosstalk between uterine natural killer (uNK) cells and trophoblast cells of the placenta [6]. Compared to wild type placentas, Adm -/- placentas exhibit fewer uNK cells and insufficient spiral artery remodeling [7].…”

Section: Introductionmentioning

confidence: 99%

Midregional pro-adrenomedullin plasma concentrations are blunted in severe preeclampsia

et al. 2014

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Levels of the peptide hormone adrenomedullin (AM) are elevated during normal pregnancy, but whether this differs during complications of pregnancy remains unresolved. AM can be quantified by measuring its preprohormone byproduct, midregional pro-adrenomedullin (MR-proADM). MR-pro ADM has shown prognostic value as a biomarker of heart failure, sepsis, and community-acquired pneumonia. Given the relevance of AM to pregnancy, we tested the hypothesis that MR-proADM provides a biomarker for preeclampsia. We find that MR-proADM plasma concentrations are blunted in severe preeclampsia and that MR-proADM is similarly effective as established biomarkers endoglin and placental growth factor at discriminating patients with severe preeclampsia from controls.

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Uterine natural killer cells as modulators of the maternal-fetal vasculature

Cited by 20 publications

References 61 publications

Restraint stress delays endometrial adaptive remodeling during mouse embryo implantation

Restraint stress delays endometrial adaptive remodeling during mouse embryo implantation

Three-dimensional cultures of trophoblast stem cells autonomously develop vascular-like spaces lined by trophoblast giant cells

Midregional pro-adrenomedullin plasma concentrations are blunted in severe preeclampsia

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