Disease relevance of Placentation

• These results identify Esx1 as the first essential X-chromosome-imprinted regulator of placental development that influences fetal growth, and may aid our understanding human placental insufficiency syndromes [1].
• This study provides the first compelling in vivo evidence that IGFBP-1 plays a role in placentation and suggests that IGFBP-1 has a pathological role in preeclampsia, a disorder characterized by shallow uterine invasion and altered placental development [2].
• beta3 integrins have been implicated in a wide variety of functions, including platelet aggregation and thrombosis (alphaIIbbeta3) and implantation, placentation, angiogenesis, bone remodeling, and tumor progression (alphavbeta3) [3].
• Mouse gene knockout studies show that an absence of either hepatocyte growth factor (HGF) or its receptor, c-met, leads to intrauterine death secondary to severe IUGR with deficient placentation [4].
• In summary P-LAP and A-LAP were predominantly expressed in the invasive phenotype of EVTs during placentation, as well as in the invasive tumor cells of trophoblastic neoplasms [5].

High impact information on Placentation

• Esx1 is an X-chromosome-imprinted regulator of placental development and fetal growth [1].
• The Hand1 bHLH transcription factor is essential for placentation and cardiac morphogenesis [6].
• The promoter region of H19 is hypomethylated at all stages of placental development, while the 3' portion shows progressive methylation of the paternal allele with gestation [7].
• Apparent role of the macrophage growth factor, CSF-1, in placental development [8].
• Targeted disruption of the murine VCAM1 gene: essential role of VCAM-1 in chorioallantoic fusion and placentation [9].

Chemical compound and disease context of Placentation

• Cerebral tissue oxygenation during hypoxia and hyperoxia using artificial placentation in lamb [10].
• Creatine kinase levels were above this cutoff in two of five unruptured ampullary ectopic pregnancies with invasive trophoblastic growth, yet in none of nine cases with intraluminally confined placentation (P = 0.04) [11].

Biological context of Placentation

• Our results demonstrate that RAP250 is necessary for placental development and thus essential for embryonic development [12].
• As early as E9.5, HAI-1-/- embryos showed growth retardation that did not reflect impaired cell proliferation but resulted instead from failed placental development and function [13].
• Trophoblast cell-specific carcinoembryonic antigen cell adhesion molecule 9 is not required for placental development or a positive outcome of allotypic pregnancies [14].
• Cyclin F disruption compromises placental development and affects normal cell cycle execution [15].
• The expression and function of cystatin C and cathepsin B and cathepsin L during mouse embryo implantation and placentation [16].

Anatomical context of Placentation

• Thus, this interaction between maternal KIR and trophoblast appears not to have an immune function, but instead plays a physiological role related to placental development [17].
• Role of uterine natural killer cells and interferon gamma in placental development [18].
• Rescue of the implantation defect by tetraploid fusion established that Cdx2 is necessary for trophoblastic development, vasculogenesis in the yolk sac mesoderm, allantoic growth, and chorioallantoic fusion. "Rescued" Cdx2 mutants die at late gastrulation stages because of failure of placental development [19].
• Last, variably penetrant maternal blood sinus dilation in Muc1-deficient placentas suggests that Muc1 regulation by PPARgamma contributes to normal placental development but also that the essential functions of PPARgamma in the organ are mediated by other targets [20].
• In the extraembryonic region, syndecan is not detectable on most cells of the central core of the ectoplacental cone, but is strongly expressed by cells undergoing trophoblast giant cell differentiation and remains prominent on differentiated giant cells, suggesting a role in placental development [21].

Associations of Placentation with chemical compounds

• These findings indicate that CSF-1, under hormonal influence, plays a role in placental development and function and that steroid hormones may regulate developmental processes via their effects on the expression of tissue-specific growth factors [8].
• This result suggests that the variation in placentation has a significant effect on within-pair variation in serum cholesterol of newborn MZ twins [22].
• Placental development initially occurs in a low-oxygen (O2) or hypoxic environment [23].
• If receptor expression is similarly genetically determined in the placenta, responsiveness to angiotensin II may be affected, with the potential to influence placentation or placental prostaglandin secretion [24].
• In order to investigate the possible role of retinoic acid (RA) in placentation, we analyzed the effects of exogenous RA on TS cells in vitro and the developing ectoplacental cone in vivo [25].

Gene context of Placentation

• Targeted disruption of both alleles of mouse sos1, which encodes a Ras-specific exchange factor, conferred mid-gestational embryonic lethality that was secondary to impaired placental development and was associated with very low placental ERK activity [26].
• Here, we investigated the placental development in Flt1-deficient mice [27].
• The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma) is essential for placental development [20].
• Loss of Cited1 resulted in abnormal placental development [28].
• Wnt7b is a Wnt ligand that has been demonstrated to play critical roles in several developmental processes, including lung airway and vascular development and chorion-allantois fusion during placental development [29].

Analytical, diagnostic and therapeutic context of Placentation

• Estrone (E1) and 17 beta-estradiol (17 beta-E2) serum levels increase with placental development; after hysterectomy, they are low from days 12-168 [30].
• Northern blot analysis revealed that large amounts of IP-10 mRNA were present during conceptus attachment to maternal endometrium and early placentation [31].
• Our results indicate that only PIH/PE with poor pregnancy outcome is associated with defective placentation, whereas PIH/PE with good outcome is not [32].
• However, in mares carrying failing donkey-in-horse pregnancies created by embryo transfer, EGF expression was severely retarded in those areas of the endometrium that were heavily infiltrated with lymphocytes and which showed a failure of placental development [33].
• We carried out comparative analyses of the location and identity of the cells expressing Hoxc-9/HOXC-9 during various stages of placentation in the murine hemochorial and caprine synepitheliochorial placentae by means of in situ hybridization using murine Hoxc-9 or caprine HOXC-9 cRNA probe, respectively [34].

References