Vascular Endothelial Growth Factor is a Chemoattractant for Trophoblast Cells

Lash, Gendie E.; Warren, Averil Y.; Underwood, Suzanne; Baker, Philip N.

doi:10.1053/plac.2002.0923

Cited by 37 publications

(21 citation statements)

References 27 publications

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“…Furthermore, a dialogue between embryo and endometrium is considered essential for blastocyst implantation and may involve the synthesis and secretion of hCG and VEGF from embryonic and maternal sources respectively (Licht et al 2001). Several reported studies earlier indicated a possible role of VEGF in the regulation of invasive and migratory capacities of early placental trophoblasts (Lash et al 2003, Anteby et al 2004. Thus, it appears that the observed high incidence of pregnancy failure following anti-VEGF Mab treatment might have been precipitated by inadequate trophoblast invasion and placental formation associated with their lower expression of VEGF, KDR, and FLT-1.…”

Section: Discussionmentioning

confidence: 99%

Immunoneutralization of vascular endothelial growth factor inhibits pregnancy establishment in the rhesus monkey (Macaca mulatta)

Sengupta¹,

Lalitkumar²,

Najwa³

et al. 2007

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Section: Discussionmentioning

confidence: 99%

Immunoneutralization of vascular endothelial growth factor inhibits pregnancy establishment in the rhesus monkey (Macaca mulatta)

Sengupta¹,

Lalitkumar²,

Najwa³

et al. 2007

Reproduction

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“…In vitro studies showed that heparin is a modulator of the heparin-binding-endothelial growth factor (EGF) and the vascular endothelial growth factor (VEGF). 30,31 In preeclampsia, reduced levels and activity of growth factors, such as VEGF, placental growth factor, and HB-EGF, involved in the trophoblast differentiation and invasion have been demonstrated. 32,33 Previous studies 8 -11,34 showed decreased pregnancy complications in thrombophilic women associated with unfractionated and LMWH administration.…”

Section: Discussionmentioning

confidence: 99%

Low-Molecular-Weight Heparin Lowers the Recurrence Rate of Preeclampsia and Restores the Physiological Vascular Changes in Angiotensin-Converting Enzyme DD Women

et al. 2005

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Abstract-Data from literature report that angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism affects the recurrence of preeclampsia and that low-molecular-weight heparin (LMWH) prevents adverse outcomes in thrombophilic women. We investigated the effect of LMWH on the pregnancy outcome, on maternal blood pressure values, and on uteroplacental flow in ACE DD nonthrombophilic women with history of preeclampsia. Eighty nonthrombophilic ACE DD women were randomized in 2 groups: 41 treated with dalteparin 5000 IU/day and 39 untreated (control group). Women underwent 24-hour automated blood pressure monitoring in the preconceptional period and every 2 weeks from weeks 8 to 36 and transabdominal color flow/pulsed Doppler examination at weeks 16, 20, and 24. LMWH reduced the risk of clinical negative outcomes (74.1% reduction of preeclampsia and 77.5% reduction of fetal growth restriction) and the severity (88.3% reduction of early onset of preeclampsia and 86.4% reduction of early onset of fetal growth restriction). In treated women, the relative risk for preeclampsia was 0.26 (Pϭ0.02), and the relative risk for fetal growth restriction was 0.14 (PϽ0.001). Systolic (Pϭ0.002) and diastolic (Pϭ0.002) blood pressures, as well as awake (Pϭ0.04) and asleep (Pϭ0.01) period values, and the resistance indexes of both uterine arteries (Pϭ0.002) were lower in the treated group. LMWH reduces the recurrence of preeclampsia, of negative outcomes, and the resistance of uteroplacental flow, and also prevents maternal blood pressure increase in ACE DD homozygote women with a previous history of preeclampsia.

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“…53,54 Other studies suggest that heparins are involved in the adhesion of the blastocyst to the endometrial epithelium, and its subsequent invasion, and that they have the capacity to interfere with blastocyst-uterine cross talk during implantation. 55 Additionally, heparin therapies could minimize the damage caused by antiphospholipid antibodies by altering the binding of antiphospholipid antibodies to phospholipids on target cells and/or limiting the binding of β 2 GPI to phospholipids, which would prevent targeting by, and deposition of, anti-β 2 GPI antibodies.…”

Section: Prevention Of Fetal and Placental Injury By Heparinmentioning

confidence: 99%

The antiphospholipid syndrome as a disorder initiated by inflammation: implications for the therapy of pregnant patients

2007

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Arterial thrombosis, venous thrombosis and morbidity during pregnancy, or a combination of these events, are clinical outcomes associated with antiphospholipid antibodies produced by patients with antiphospholipid syndrome (APS). Our understanding of the etiology and pathogenesis of the syndrome is limited, but it has generally been considered a thrombophilic disease and treatment has focused on anticoagulation. Agents such as aspirin and heparin, administered alone or in combination, are empirical treatments that are used in the management of obstetric patients with APS. Clinical features, such as heart valve abnormalities, thrombocytopenia and livedo reticularis, suggest multiple pathogenic mechanisms and provide other therapeutic targets. Findings from research in animal models of APS challenge the dogma that this syndrome is a noninflammatory, thrombotic disease and provide evidence that activation of complement is crucial for complications in pregnancy. These studies, in addition to evidence of inflammatory-mediated tissue damage in placentae of patients with APS, suggest that therapy should also be directed towards preventing inflammation. This Review describes the potential mechanisms of tissue injury by antiphospholipid antibodies, the management of pregnant patients with APS and how heparin therapy might inhibit the pathogenic mediators of disease.

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Vascular Endothelial Growth Factor is a Chemoattractant for Trophoblast Cells

Cited by 37 publications

References 27 publications

Immunoneutralization of vascular endothelial growth factor inhibits pregnancy establishment in the rhesus monkey (Macaca mulatta)

Immunoneutralization of vascular endothelial growth factor inhibits pregnancy establishment in the rhesus monkey (Macaca mulatta)

Low-Molecular-Weight Heparin Lowers the Recurrence Rate of Preeclampsia and Restores the Physiological Vascular Changes in Angiotensin-Converting Enzyme DD Women

The antiphospholipid syndrome as a disorder initiated by inflammation: implications for the therapy of pregnant patients

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