Implantation of the mammalian embryo requires profound endometrial changes for successful pregnancy, including epithelial-mesenchymal transition of the luminal epithelium and stromal-epithelial transition of the stromal cells resulting in decidualization. Claudins (Cldn) determine the variability in tight junction paracellular permeability and may play a role during these epithelial and decidual changes. We here localized Cldn3, Cldn7 and Cldn10 proteins in the different compartments of murine endometrium up to day 8.5 of pregnancy (dpc) as well as in human endometrium and first trimester decidua. In murine estrous endometrium, luminal and glandular epithelium exhibited Cldn3 and Cldn7, whereas Cldn10 was only detectable in glandular epithelium. At 4.5 dpc, Cldn3 protein shifted to an apical localization, whereas Cldn7 vanished in the epithelium of the implantation chamber. At this stage, there was no stromal signal for Cldn3 and Cldn7, but a strong induction of Cldn10 in the primary decidual zone. Cldn3 proteins emerged at 5.5 dpc spreading considerably from 6.5 dpc onward in the endothelial cells of the decidual blood sinusoids and in the decidual cells of the compact antimesometrial region. In addition to Cldn3, Cldn10 was identified in human endometrial epithelia. Both proteins were not detected in human first trimester decidual cells. Cldn3 was shown in murine trophoblast giant cells as well as in human extravillous trophoblast cells and thus may have an impact on trophoblast invasion in both species. We here showed a specific claudin signature during early decidualization pointing to a role in decidual angiogenesis and regulation of trophoblast invasion.
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http://dx.doi.org/10.1007/s00418-015-1361-z | DOI Listing |
Am J Case Rep
January 2025
Department of Pathology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
BACKGROUND Gestational trophoblastic diseases (GTDs) are a group of benign and malignant tumors that arise from placental tissue. Ectopic pregnancies most commonly occur within the fallopian tubes. The estimated incidence of ectopic gestational trophoblastic diseases (GTDs) is approximated at 1.
View Article and Find Full Text PDFIr J Med Sci
January 2025
Department of Obstetrics and Gynecology, Perinatology Clinic, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul, Turkey.
Background: Sirtuins and FoxO1 are reported to be important in the pathophysiology of preeclampsia. This study aimed to investigate whether serum FoxO1 and SIRT2 concentrations differ between preeclampsia and normal pregnancy and also to compare these markers in early- and late-onset preeclampsia.
Methods: This cross-sectional study was conducted on 27 women with early-onset preeclampsia, 27 women with late-onset preeclampsia, and 26 healthy normotensive pregnant controls.
Biol Reprod
January 2025
Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, CO USA.
The mechanistic target of rapamycin (mTOR) system is vital to placental development, formation, and function. Alterations in this system in the placenta have been associated with altered fetal growth. However, changes in placental mTOR signaling across gestation are poorly understood.
View Article and Find Full Text PDFClin Chim Acta
January 2025
Biochemistry Department, Centro Universitário Faculdade de Medicina ABC (FMABC), Santo André, São Paulo, Brazil.
Preeclampsia (PE) is a gestational complication affecting 5% to 10% of all pregnancies. PE is characterized by hypertension and endothelial dysfunction, whose etiology involves, among other factors, alterations in the extracellular matrix (ECM) that can compromise vascular remodeling and trophoblast invasion, ie, processes essential for placental development. Endothelial dysfunction is caused by release of antiangiogenic factors, mainly a soluble fms-like tyrosine kinase-1 (sFlt-1), which antagonizes two endothelial angiogenic factors, the vascular endothelial growth factor (VEGF) and placental growth factor (PLGF).
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Reproductive Biology Laboratory, Amsterdam University Medical Center Location University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Placentation disorders, including severe preeclampsia and fetal growth restriction, have their origins in early pregnancy, whereas symptoms typically present later on. To investigate the pathogenesis of these diseases, there is a need for a reliable in vitro model system of early placenta development with known pregnancy outcomes. Therefore, we optimized the generation of human induced trophoblast stem cells (iTSCs) from term umbilical cord, enabling non-invasive collection of patient-derived material immediately after birth.
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