A Vascular Endothelial Growth Factor Antagonist Is Produced by the Human Placenta and Released into the Maternal Circulation
. Biol Reprod.
In addition to understanding the impact of EDCs on GDM, it is our hope that miRNAs in maternal circulation
will serve as a noninvasive biomarker for early detection of GDM development or susceptibility.
[30,31] This is most active in the presence of higher concentration gradient of this metal in maternal circulation
. The lower level in our study possibly explains why we observed higher maternal mercury levels than in cord blood.
However, delivery can lead to sharp increase in maternal serum calcium levels as the calcium, which had previously been preferentially received by the fetus, now remains solely in maternal circulation
. Additionally, the neonate may experience significant hypocalcemic crisis and tetany after delivery as its PTH levels are suppressed and previously maternally supplied calcium disappears [1, 3].
leptin, inflammation, lipids and fatty acids levels) in maternal circulation
were not measured in current study.
Abnormalities in maternal circulation
(maternal vascular malperfusion) can lead to fetoplacental unit underperfusion and FVM.
It was established over 20 years ago that fetal cells were detectable in the maternal circulation
often as early as six weeks' gestation (58) and that fetal DNA can be detected in the maternal circulation
giving rise to speculation that this discovery could lead to the development of noninvasive prenatal diagnosis (59).
How stable is microbial plasma cfRNA in the maternal circulation
? And how can we standardize criteria for microbial detection and classification given that results are highly dependent on experimental and data analysis protocols (11)?
 Xanthine oxidase is thought to play a fundamental role in free radical induced tissue damage in human placenta and as a result of under-perfusion, necrotic processes could lead to discharge syncytiotrophoblast microvesicles into maternal circulation
. These microparticles present in the blood during pregnancy have been shown to increase in concentration in pre-eclampsia and have been directly involved in activation of maternal neutrophils, which in turn might contribute to activation of the vascular endothelium.
Mother may be sensitized to the Kell antigen by two predominant mechanisms: transfusion from a Kell-positive donor or by fetal hemorrhage of Kell-positive blood in to the maternal circulation
. Transplacental sensitization occurred in almost half (51%) of a series of 65 pregnancies, with 45% having a history of maternal transfusion .
During pregnancy, due to a normal extravillous trophoblast invasion, nucleic acids of the placental compartment are released into the maternal circulation
: this release occurs through the migration of microvesicles from apoptotic/necrotic cells and active cellular communication system, involving also nanovesicles/exosomes and subcellular fragments [18, 19].
At delivery, this plasma expansion is increased further by the return of the uteroplacental blood to the maternal circulation
, increased systemic vascular resistance, pain, and exclusion of the low vascular resistance of the placental system.