Exploring the Lifeline: Unpacking the Complexities of Placental Vascular Function in Normal and Preeclamptic Pregnancies.

The proper development and function of the placenta are essential for the success of pregnancy and the well-being of both the fetus and the mother. Placental vascular function facilitates efficient fetal development during pregnancy by ensuring adequate gas exchange with low vascular resistance. This review focuses on how placental vascular function can be compromised in the pregnancy pathology preeclampsia, and conversely, how placental vascular dysfunction might contribute to this condition.

In vitro examination of Piezo1-TRPV4 dynamics: implications for placental endothelial function in normal and preeclamptic pregnancies.

Mechanosensation is essential for endothelial cell (EC) function, which is compromised in early-onset preeclampsia (EPE), impacting offspring health. The ion channels Piezo-type mechanosensitive ion channel component 1 (Piezo1) and transient receptor potential cation channel subfamily V member 4 (TRPV4) are coregulated mechanosensors in ECs. Current evidence suggests that both channels could mediate aberrant placental endothelial function in EPE.

Liver X receptor activation mitigates oxysterol-induced dysfunction in fetoplacental endothelial cells.

Maintaining the homeostasis of the placental vasculature is of paramount importance for ensuring normal fetal growth and development. Any disruption in this balance can lead to perinatal morbidity. Several studies have uncovered an association between high levels of oxidized cholesterol (oxysterols), and complications during pregnancy, including gestational diabetes mellitus (GDM) and preeclampsia (PE).

Synergistic regulation of uterine radial artery adaptation to pregnancy by paracrine and hemodynamic factors.

Fetal growth throughout pregnancy relies on delivery of an increasing volume of maternal blood to the placenta. To facilitate this, the uterine vascular network adapts structurally and functionally, resulting in wider blood vessels with decreased flow-mediated reactivity. Impaired remodeling of the rate-limiting uterine radial arteries has been associated with fetal growth restriction.

Serine Hydrolases in Lipid Homeostasis of the Placenta-Targets for Placental Function?

The metabolic state of pregnant women and their unborn children changes throughout pregnancy and adapts to the specific needs of each gestational week. These adaptions are accomplished by the actions of enzymes, which regulate the occurrence of their endogenous substrates and products in all three compartments: mother, placenta and the unborn. These enzymes determine bioactive lipid signaling, supply, and storage through the generation or degradation of lipids and fatty acids, respectively.

Pregnancy-specific uterine vascular reactivity: a data-driven computational model of shear-dependent, myogenic, and mechanical radial artery features.

`The entire maternal circulation adapts to pregnancy, and this adaption is particularly extensive in the uterine circulation where the major vessels double in size to facilitate an approximately 15-fold increase in blood supply to this organ over the course of pregnancy. Several factors may play a role in both the remodeling and biomechanical function of the uterine vasculature including the paracrine microenvironment, passive properties of the vessel wall, and active components of vascular function (incorporating the myogenic response and response to shear stress induced by intravascular blood flow). However, the interplay between these factors and how this plays out in an organ-specific manner to induce the extent of remodeling observed in the uterus is not well understood.

From stem cells to spiral arteries: A journey through early placental development.

Early placental development lays the foundation of a healthy pregnancy, and numerous tightly regulated processes must occur for the placenta to meet the increasing nutrient and oxygen exchange requirements of the growing fetus later in gestation. Inadequacies in early placental development can result in disorders such as fetal growth restriction that do not present clinically until the second half of gestation. Indeed, growth restricted placentae exhibit impaired placental development and function, including reduced overall placental size, decreased branching of villi and the blood vessels within them, altered trophoblast function, and impaired uterine vascular remodelling, which together combine to reduce placental exchange capacity.

Something old, something new: digital quantification of uterine vascular remodelling and trophoblast plugging in historical collections provides new insight into adaptation of the utero-placental circulation.

Study Question: What is the physiological extent of vascular remodelling in and trophoblast plugging of the uterine circulation across the first half of pregnancy?

Summary Answer: All levels of the uterine vascular tree (arcuate, radial and spiral arteries (SAs)) dilate ∼2.6- to 4.3-fold between 6 and 20 weeks of gestation, with significant aggregates of trophoblasts persisting in the decidual and myometrial parts of SAs beyond the first trimester.

Expression of angiogenic factors in the uteroplacental unit is altered at time of placentation in a porcine model of von Willebrand disease type 1.

Von Willebrand disease (VWD) affects blood coagulation and correlates with angiodysplasia. Data on VWD-affected women point to slightly increased miscarriage rates. We aimed to investigate the impact of VWD on angiogenesis in the uteroplacental unit of pregnant pigs of a model of VWD type 1 (T1).

Characterization of a Porcine Model for Von Willebrand Disease Type 1 and 3 Regarding Expression of Angiogenic Mediators in the Nonpregnant Female Reproductive Tract.

Von Willebrand disease (VWD), a blood coagulation disorder, is also known to cause angiodysplasia. Hitherto, no animal model has been found with angiodysplasia that can be studied in vivo. In addition, VWD patients tend to have a higher incidence of miscarriages for reasons unknown.

A 12.3-kb Duplication Within the Gene in Pigs Affected by Von Willebrand Disease Type 3.

Von Willebrand Disease (VWD) type 3 is a serious and sometimes fatal hereditary bleeding disorder. In pigs, the disease has been known for decades, and affected animals are used as models for the human disease. Due to the recessive mode of inheritance of VWD type 3, severe bleeding is typically seen in homozygous individuals.