Matrix metalloproteinase 15 plays a pivotal role in human first trimester cytotrophoblast invasion and is not altered by maternal obesity.

Adequate anchoring of the placenta in the uterus through invasion of first trimester cytotrophoblasts (CTB) is required for a successful pregnancy. This process is mediated by matrix metalloproteinases (MMPs) and regulated by the maternal environment. Obesity is known to alter the intrauterine milieu and has been related to impaired invasion.

Endothelin-1 down-regulates matrix metalloproteinase 14 and 15 expression in human first trimester trophoblasts via endothelin receptor type B.

Study Question: Does endothelin-1 (ET-1) regulate matrix metalloproteinase (MMP) 14 and 15 production and invasion of human first trimester trophoblasts?

Summary Answer: ET-1 in pathophysiological concentrations down-regulates MMP14 and MMP15 expression via endothelin receptor (ETR) type B and decreases trophoblast migration and invasion.

What Is Known Already: MMP14 and MMP15 are involved in trophoblast invasion. Impairment of invasion has been linked to pregnancy complications such as pre-eclampsia (PE).

Individual Human Metabolic Phenotype Analyzed by (1)H NMR of Saliva Samples.

Saliva is an important physiological fluid that contains a complex mixture of analytes that may produce a characteristic individual signature. In recent years, it has been demonstrated that urine possesses a clear signature of the individual metabolic phenotype. Here NMR-based metabolomics was employed to analyze saliva from 23 healthy volunteers.

Placental fractalkine is up-regulated in severe early-onset preeclampsia.

The pathogenesis of preeclampsia (PE) includes the release of placental factors into the maternal circulation, inducing an inflammatory environment in the mother. One of the factors may be the proinflammatory chemokine fractalkine, which is expressed in the syncytiotrophoblast of human placenta, from where it is released into the maternal circulation by constitutive shedding. We examined whether placental fractalkine is up-regulated in severe early-onset PE and whether the proinflammatory cytokines tumor necrosis factor (TNF)-α and IL-6 are able to increase the expression of fractalkine.

The impact of free or standardized lifestyle and urine sampling protocol on metabolome recognition accuracy.

Urine contains a clear individual metabolic signature, although embedded within a large daily variability. Given the potential of metabolomics to monitor disease onset from deviations from the "healthy" metabolic state, we have evaluated the effectiveness of a standardized lifestyle in reducing the "metabolic" noise. Urine was collected from 24 (5 men and 19 women) healthy volunteers over a period of 10 days: phase I, days 1-7 in a real-life situation; phase II, days 8-10 in a standardized diet and day 10 plus exercise program.

Molecular mechanisms of endometrial stromal sarcoma and undifferentiated endometrial sarcoma as premises for new therapeutic strategies.

Endometrial stromal sarcoma (ESS) and undifferentiated endometrial sarcoma (UES) are very rare gynecologic malignancies. Due to the rarity and heterogeneity of these tumors, little is known about their epidemiology, pathogenesis, and molecular pathology. Our previous studies have described deregulation of histone deacetylases expression in ESS/UES samples.

Membrane-type matrix metalloproteinase 1 regulates trophoblast functions and is reduced in fetal growth restriction.

Fetal growth restriction (FGR) results from placental insufficiency to adequately supply the fetus. This insufficiency involves impaired cytotrophoblast functions, including reduced migration and invasion, proliferation, and syncytium formation. Membrane-type matrix metalloproteinase 1 (MT1-MMP) is a key enzyme in these cellular processes.

Complex expression changes of the placental endothelin system in early and late onset preeclampsia, fetal growth restriction and gestational diabetes.

Aims: Preeclampsia (PE), fetal growth restriction (FGR) and gestational diabetes mellitus (GDM) are major pregnancy complications affecting maternal and fetal health. The placenta and the vasoconstrictor endothelin-1 (ET-1) have a controlling and mediating role in these conditions. This study tested the hypothesis that the expression of ET-1 and its receptors (ET(A) and ET(B)) is altered in these pathologies and differs between early (gestational week [GW] ≤ 34) and late (GW > 34) third trimester pregnancies.

Phospholipid transfer protein in the placental endothelium is affected by gestational diabetes mellitus.

Context: Gestational diabetes mellitus (GDM) causes alterations in fetal high-density lipoproteins (HDL). Because phospholipid transfer protein (PLTP) is important for HDL (re)assembly and is expressed in the human placenta, we hypothesized that circulating fetal and/or placental PLTP expression and activity are altered in GDM.

Design: PLTP levels and activity were determined in maternal and fetal sera from GDM and controls.

Up-regulation of the endothelin receptor A in placental tissue from first trimester delayed miscarriages.

Objective: This study tested the hypothesis that the endothelin (ET)/ET receptor (ETR) system in biologic fluids and in the human placenta is altered in delayed miscarriages as compared to apparently normal early pregnancies (reference group).

Methods: Immunoreactive ET (irET) concentrations were measured in plasma, urine, and cervical smears from 57 pregnant women in the weeks 6 to 14 of gestation (46 delayed miscarriages, 11 references) with radioimmunoassay (RIA). ET-1, ETR-A, and ETR-B mRNA, and ETR protein expression were measured in placental tissue of 45 early pregnancies (31 delayed miscarriages, 14 references) using semiquantitative reverse-transcription polymerase chain reaction (RT-PCR) and immunoblotting, respectively.