Phosphoglycoprotein (P-gp) is highly expressed in the placental syncytiotrophoblast and prevents xenobiotics from entering the fetus. In tumor cells, P-gp-mediated substrate efflux is inhibited by selective serotonin reuptake inhibitors (SSRIs). However, nothing is known regarding the effects of SSRIs on P-gp function in the placenta or fetal tissues. We hypothesized that the SSRI sertraline would decrease P-gp-mediated drug efflux at the placenta and fetal blood-brain barrier (BBB)-increasing P-gp substrate transfer from the mother to the fetus and fetal brain. In contrast to our hypothesis, this study presents the novel findings that sertraline (4 hours exposure) increases placental P-gp-mediated efflux (P < .001), resulting in decreased drug transfer to the fetus. Meanwhile, sertraline decreases fetal (P < .001) and maternal (P < .05) BBB P-gp-mediated efflux, resulting in increased drug transfer into the fetal and maternal brain from the circulation. This suggests that P-gp regulation by sertraline is tissue specific. These findings have important clinical implications with respect to fetal protection during maternal drug therapy in pregnancy.
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http://dx.doi.org/10.1177/1933719111424438 | DOI Listing |
Neurotoxicol Teratol
January 2025
Center for the Prevention of Preterm Birth, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, United States; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, United States; Office of the President, Burroughs Wellcome Fund, Research Triangle Park, Durham, NC, United States. Electronic address:
Exposure to psychosocial stress during pregnancy has been associated with the emergence of neurodevelopmental and neuropsychiatric disorders in offspring. The placenta is known to orchestrate various functions that are essential for normal fetal development, including the brain. It has therefore been postulated that alterations in such functions, and downstream signaling, have the potential to dramatically affect brain developmental trajectories and contribute to adverse neurodevelopmental outcomes.
View Article and Find Full Text PDFPlacenta
December 2024
Seattle Children's Research Institute, Seattle WA, USA; University of Washington, Seattle WA, USA.
Introduction: The placenta produces corticotrophin releasing hormone (CRH), which rises exponentially in maternal plasma across pregnancy. CRH plays a functional role in fetal development, labor initiation, and the regulation of gestational length. We aimed to understand how maternal plasma CRH during pregnancy reflects placental physiology during parturition by characterizing placental transcriptomic signatures of maternal plasma CRH and comparing to transcriptomic signatures of gestational age at birth.
View Article and Find Full Text PDFHum Cell
January 2025
Department of Metabolism and Endocrinology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
The escalating diabetes prevalence has heightened interest in innovative therapeutic strategies for this disease and its complications. Human amniotic epithelial stem cells (HAESCs), originate from the innermost layer of the placenta closest to the fetus and express stem cell markers in the amniotic membrane's umbilical cord attachment area, which have garnered significant attention. This article critically examines emerging research advancements and potential application values of hAESCs in treating diabetes and its complications.
View Article and Find Full Text PDFNat Commun
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 PDFJ Obstet Gynaecol Res
January 2025
Pregnancy Research Centre, Department of Maternal Fetal Medicine, the Royal Women's Hospital, Parkville, Victoria, Australia.
Aim: To evaluate if maternal serum soluble fms-like tyrosine kinase-1(sFlt-1) to placental growth factor (PlGF) ratio levels at term can anticipate the following adverse pregnancy outcomes: small for gestational age neonates; operative delivery for suspected fetal welfare compromise; and neonatal compromise.
Methods: A retrospective analysis of a single hospital database containing antenatal soluble fms-like tyrosine kinase-1 to placental growth factor (sFlt-1/PlGF) ratio results together with associated demographic, clinical and investigative information. Subjects with antenatal sFlt-1/PlGF measurements taken ≥37 weeks' gestation were analyzed.
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