Deep placentation in the human requires physiologic transformation of the spiral arteries into uteroplacental vessels. This process involves the inner myometrial segment (junctional zone) of the spiral arteries and is effected by trophoblast invasion of the vessel wall, resulting in complete loss of the arterial structure and deposition of fibrinoid and fibrous tissues. Absent or inadequate physiologic changes in the junctional zone spiral arteries limits placental blood flow in pregnancies complicated by preeclampsia and fetal growth restriction. The cause of defective deep placentation is still unknown, although it is often attributed to impaired trophoblast function and migration. However, trophoblast invasion is preceded by decidual remodeling of maternal tissues, a process that is initiated in the endometrium but extends into the junctional zone. This review examines the mechanisms that control decidualization and subsequent trophoblast invasion in normal and abnormal pregnancies. The possibility that disruption of the decidual process in the secretory phase of the menstrual cycle triggers a cascade of events resulting in failed deep placentation is explored.
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http://dx.doi.org/10.1067/mob.2002.127305 | DOI Listing |
To assess the repeatability of a microperimetry methodology for quantifying visual function changes in the junctional zone of eyes with geographic atrophy (GA) in the clinical trial context. A post hoc analysis of the OAKS phase III trial was conducted, which enrolled patients with GA secondary to age-related macular degeneration. Microperimetry using a standard 10-2 fovea centered grid was performed at baseline and follow-up visits.
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January 2025
Department of Obstetrics and Gynaecology, University of Cambridge, NIHR Cambridge Biomedical Research Centre, Cambridge, United Kingdom.
The placenta is the critical interface between mother and fetus, and consequently, placental dysfunction underlies many pregnancy complications. Placental formation requires an adequate expansion of trophoblast stem and progenitor cells followed by finely tuned lineage specification events. Here, using single-cell RNA sequencing of mouse trophoblast stem cells during the earliest phases of differentiation, we identify gatekeepers of the stem cell state, notably Nicol1, and uncover unsuspected trajectories of cell lineage diversification as well as regulators of lineage entry points.
View Article and Find Full Text PDFSci Rep
December 2024
Robinson Research Institute, School of Biomedicine, University of Adelaide, Adelaide, SA, Australia.
Studies in humans and rodents show exercise in pregnancy can modulate maternal blood pressure, vascular volume, and placental efficiency, but whether exercise affects early uteroplacental vascular adaptations is unknown. To investigate this, CBA/J female mice mated with BALB/c males to generate healthy uncomplicated pregnancies (BALB/c-mated) or mated with DBA/2J males to generate abortion-prone pregnancies (DBA/2J-mated), were subjected to treadmill exercise (5 days/week, 10 m/min, 30 min/day for 6 weeks before and throughout pregnancy), or remained sedentary. In uncomplicated pregnancies, exercise caused symmetric fetal growth restriction in fetuses evidenced by reductions in fetal weight, crown-to-rump length, abdominal girth and biparietal diameter.
View Article and Find Full Text PDFCureus
November 2024
Radiodiagnosis, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, IND.
Abnormal uterine bleeding (AUB) is a common gynecological condition that disrupts women's health due to irregularities in menstrual frequency, duration, and volume, often resulting in a significant impact on daily life and productivity. Accurate diagnosis of AUB is critical but complicated by its varied etiologies and presentations. Recent advancements in imaging techniques, particularly the Morphological Uterus Sonographic Assessment (MUSA), have enhanced the diagnostic precision of uterine pathologies such as fibroids and adenomyosis.
View Article and Find Full Text PDFRedox Biol
December 2024
Baruch College and CUNY Graduate Center, 1 Baruch Way, New York, NY, 10010, USA. Electronic address:
The elevated emission of reactive oxygen species (ROS) from presynaptic mitochondria is well-documented in several inflammatory and neurodegenerative diseases. However, the potential role of mitochondrial ROS in presynaptic function and plasticity remains largely understudied beyond the context of disease. Here, we investigated this potential ROS role in presynaptic function and short-term plasticity by combining optogenetics, whole cell electrophysiological recordings, and live confocal imaging using a well-established protocol for induction and measurement of synaptic potentiation in Drosophila melanogaster neuromuscular junctions (NMJ).
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