Embryogenesis and gene targeting of coagulation factors in mice

Sood, Rashmi; Weiler, Hartmut

doi:10.1016/s1521-6926(02)00092-0

Cited by 7 publications

(8 citation statements)

References 58 publications

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“…An increased concentration of both factor V and FII during the early pregnancy stage, followed by a decrease and stabilization [39], along with a gradual rise of factor V activity throughout gestation [40] were reported. This fluctuation in the concentration not tied to activity could be explained by the important role of factor V in cell adhesion, smooth muscle proliferation and vasculogenesis and more during embryonic development [41]. The slight increase of APC (natural inhibitor of factor V) at early pregnancy could explain normal level of factor V activity at embryonic period.…”

Section: Factor V Leiden Carriage In Patients With Miscarriagementioning

confidence: 99%

“…The higher prevalence of FII 20210G>A mutation compared with FVL in women with RPL emphasized the important role of increased prothrombin levels for the development of early miscarriage. According to the investigations in knockout mice [41], FII is required to establish and maintain the integrity of blood vessels in the embryonic yolk sac. The research [46,47] on thrombin receptor showed thrombin effect upon endothelial and mesenchymal cells and its contribution to vascular development in mouse embryo.…”

Section: Fii 20210g>a Carriage In Patients With Miscarriagementioning

confidence: 99%

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Association of inherited thrombophilia with embryonic and postembryonic recurrent pregnancy loss

Ivanov¹,

Komsa-Penkova²,

Konova

et al. 2009

Blood Coagulation &Amp; Fibrinolysis

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To investigate the impact of maternal-inherited thrombophilia: effects of factor V Leiden (FVL) and prothrombin gene mutation (FII 20210G>A) on the development of recurrent pregnancy loss in embryonic and postembryonic periods. A total of 153 patients were analysed for FVL and FII 20210G>A according to placenta gestation: 94 women with embryonic loss prior 10 weeks of gestation and 59 women with postembryonic (early fetal) loss occurring between 10 and 14 weeks of gestation. The control group consisted of 100 healthy women, with at least one uncomplicated full-term pregnancy. FVL prevalence was not significantly associated with pregnancy loss prior to 10 weeks of gestation (9.6%) compared with controls (7%) [odds ratio (OR) 1.41; 95% confidence interval (CI) 0.454-4.416, P > 0.05], but it was much more pronounced in women with postembryonic loss (10-14 weeks of gestation) - 18.6% (OR 3.05; 95% CI 1.010-9.387, P = 0.047). FII 20210G>A was significantly higher in both groups with embryonic (17%) and early fetal losses (16.9%) as compared to controls (3%) (OR 6.63; 95% CI 1.731-29.752, P = 0.003; OR 6.60; 95% CI 1.572-31.856, P = 0.006). FII 20210G>A is significantly associated with an increased risk of early recurrent pregnancy loss throughout the entire first trimester. FVL was significantly higher only in early fetal period after starting of the placentation process, but not associated with embryonic recurrent pregnancy loss. These results suggested that the first trimester should be viewed rather as a heterogeneous interval, with different relation to FVL in the embryonic and postembryonic fetal period. Genetic testing should be applied according to the diverse contribution of thrombophilic markers to embryonic and postembryonic period.

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Section: Factor V Leiden Carriage In Patients With Miscarriagementioning

confidence: 99%

Section: Fii 20210g>a Carriage In Patients With Miscarriagementioning

confidence: 99%

Association of inherited thrombophilia with embryonic and postembryonic recurrent pregnancy loss

Ivanov¹,

Komsa-Penkova²,

Konova

et al. 2009

Blood Coagulation &Amp; Fibrinolysis

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“…Knockout studies in mice have identified a number of genes required for normal placentation (Cross, 2005), including genes that regulate the activity of the coagulation system (Brenner and Kupferminc, 2003;Sood and Weiler, 2003). The developmental function of the coagulation system is at least partially independent of its wellknown hemostatic function in the regulation of the fibrin-platelet interaction, as embryos simultaneously lacking fibrinogen and carrying a severe platelet defect develop normally (Camerer et al, 2004;Palumbo et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

p45NF-E2 represses Gcm1 in trophoblast cells to regulate syncytium formation, placental vascularization and embryonic growth

et al. 2011

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SUMMARYAbsence of the leucine zipper transcription factor p45NF-E2 results in thrombocytopenia, impaired placental vascularization and intrauterine growth restriction (IUGR) in mice. The mechanism underlying the p45NF-E2-dependent placental defect and IUGR remains unknown. Here, we show that the placental defect and IUGR of p45NF-E2 (Nfe2) null mouse embryos is unrelated to thrombocytopenia, establishing that embryonic platelets and platelet-released mediators are dispensable for placentation. Rather, p45NF-E2, which was hitherto thought to be specific to hematopoietic cells, is expressed in trophoblast cells, where it is required for normal syncytiotrophoblast formation, placental vascularization and embryonic growth. Expression of p45NF-E2 in labyrinthine trophoblast cells colocalizes with that of Gcm1, a transcription factor crucial for syncytiotrophoblast formation. In the absence of p45NF-E2, the width of syncytiotrophoblast layer 2 and the expression of Gcm1 and Gcm1-dependent genes (Synb and Cebpa) are increased. In vitro, p45NF-E2 deficiency results in spontaneous syncytiotrophoblast formation, which can be reversed by Gcm1 knockdown. Increased Gcm1 expression in the absence of p45NF-E2 is dependent on enhanced protein acetylation, including post-translational modification of Gcm1. Increasing and inhibiting acetylation in the placenta of wild-type control embryos phenocopies and corrects, respectively, the changes observed in p45NF-E2-deficient embryos. These studies identify a novel function of p45NF-E2 during placental development: in trophoblast cells, p45NF-E2 represses Gcm1 and syncytiotrophoblast formation via acetylation.

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“…B oth genetic and acquired thrombophilia of the pregnant mother have been associated with the occurrence of gestational vascular disease and recurrent fetal loss and may contribute to the etiology of preeclampsia. 1 Thrombomodulin is a critical cofactor in the initiation of the protein C (PC) anticoagulant pathway. 2 Plasma levels of thrombomodulin are regulated on a genetic basis, but more important is the dependence on a series of other atherosclerotic risk factors, such as hypertriglyceridemia, stroke, cancer, and diabetes.…”

Section: Data Miningmentioning

confidence: 99%

Correlation Between Thrombomodulin and Severe Preeclampsia: A Summary

Wiwanitkit¹

2008

Clin Appl Thromb Hemost

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Thrombomodulin is a critical cofactor in the initiation of the protein C anticoagulant pathway. Plasma levels of thrombomodulin are regulated on a genetic basis, but more important is the dependence on a series of other atherosclerotic risk factors, such as hypertriglyceridemia, stroke, cancer, and diabetes. There is considerable controversy regarding the clinical role of thrombomodulin level as a risk factor of severe preeclampsia. A retrospective analysis of recent reports on the thrombomodulin level and its correlation to preeclampsia was performed to assess the correlation between the pattern of thrombomodulin level and preeclampsia. From the available 4 case-control studies, 149 patients and 120 controls are evaluated. The overall average thrombomodulin level for the patients and controls is 66.7+/-11.9 ng/mL and 45.7+/-7.3 ng/mL, respectively, which is significantly higher in patients than in controls (P< .05). In addition, the author reports a significant correlation between population ethnicity and thrombomodulin level (r= .96; P< .05).

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Embryogenesis and gene targeting of coagulation factors in mice

Cited by 7 publications

References 58 publications

Association of inherited thrombophilia with embryonic and postembryonic recurrent pregnancy loss

Association of inherited thrombophilia with embryonic and postembryonic recurrent pregnancy loss

p45NF-E2 represses Gcm1 in trophoblast cells to regulate syncytium formation, placental vascularization and embryonic growth

Correlation Between Thrombomodulin and Severe Preeclampsia: A Summary

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