bims-placeb 2026-05-17 papers

bims-placeb

Biomed News

on Placental cell biology

Issue of 2026–05–17
fifteen papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences

Placental Secretome: Uncovering the Vast Signals Shaping Fetal Metabolic Health Trajectory.
The KISS1/KISS1R Axis in Human Placentation: Molecular Mechanisms and Implications for Foetal Growth Restriction and Pre-Eclampsia.
Placental Lesions in CD-1 Mouse Placenta Following Gestational Exposure to Perfluorooctanoic Acid (PFOA) or Hexafluoropropylene Oxide Dimer Acid (HFPO-DA or GenX).
Recent innovations in placental MRI: Integrating visualization and functional imaging.
Assessing Mitochondrial Respiratory Complex-Associated Function From Previously Frozen Mouse Placental Tissue.
Select Histochemical and Immunohistochemical Methods to Investigate the Cell and Tissue Composition of the Mouse Placenta and Metrial Gland.
Tryptophan's Journey Through Pregnancy: The Role of Serotonin.
Beyond Neurobiology: Cellular Prion Protein (PRNP) as an Emerging Regulator of Decidual and Utero-Placental Vascular Function.
Defective O-fucosylation of EDIL3 attenuates invasion and vascular remodeling of trophoblasts via LIFR signaling pathway in preeclampsia.
Clearing for insight: A light-sheet microscopy workflow for 3D vascular reconstruction in human first trimester placental villi and decidua.
Disturbances of the Placenta-Brain Axis in Germ-Free Pregnant Mice.
Stem Cell-based Embryo Models as a tool for reproductive biology.
Uterine fluid EV miR-223-3p as endometrial receptivity biomarker and regulator in implantation.
Conserved pathogenesis of ancestral and contemporary Oropouche virus strains in a murine pregnancy model.
Clinical Considerations for Implementing Placental Growth Factor-based testing in Urban and Rural regions in Canada.

Curr Opin Physiol. 2026 Jun;pii: 100944. [Epub ahead of print]48

Placental Secretome: Uncovering the Vast Signals Shaping Fetal Metabolic Health Trajectory.

Seokwon Jo, Emilyn U Alejandro, Megan Beetch.

  Predisposition to metabolic disease may start during pregnancy, when the intrauterine environment profoundly influences fetal development. The placenta secretes an array of proteins, hormones, metabolites, and extracellular vesicles that coordinate maternal adaptation and fetal development. Beyond classical hormones, emerging evidence reveals a broader placental secretome that regulates metabolic tissue maturation and programming. Maternal health dynamically shapes placental signaling, influencing fetal growth and long-term health trajectory. Advances in proteomics, organoids, and maternal-fetal sampling uncover secretion patterns and networks critical for fetal health programming. Understanding how the placental secretome shapes offspring health trajectories provides a crucial window for intervention to stop the intergenerational cycle of metabolic disease.

Keywords:  DOHaD; Hormone; Metabolism; Placenta; Secretome

DOI:  https://doi.org/10.1016/j.cophys.2026.100944
Int J Mol Sci. 2026 Apr 23. pii: 3748. [Epub ahead of print]27(9):

The KISS1/KISS1R Axis in Human Placentation: Molecular Mechanisms and Implications for Foetal Growth Restriction and Pre-Eclampsia.

Elitsa Gyokova, Eleonora Hristova-Atanasova, Kamelia Dimitrova.

  Pre-eclampsia and foetal growth restriction (FGR) are major pregnancy complications primarily driven by placental dysfunction, and remain leading causes of maternal and perinatal morbidity. Ultrasound imaging, Doppler studies, and angiogenic biomarkers like placental growth factor (PlGF) and soluble fms-like tyrosine kinase-1 (sFlt-1) constitute the main diagnostic modalities; however, these predominantly reflect established disease rather than early molecular disturbances underlying placentation. The identification of biomarkers directly associated with trophoblast signalling pathways has the potential to improve early risk stratification and enable mechanistic classifications. Kisspeptin signalling via its receptor (KISS1R) regulates trophoblast invasion, extracellular matrix remodelling, ERK1/2 activation, and angiogenic balance, thereby modulating spiral artery transformation. Kisspeptin-10 (KP-10), the minimal bioactive fragment of KISS1, is highly expressed in placental syncytiotrophoblasts and exerts its effects through the G-protein-coupled receptor KISS1R. Core features of early-onset FGR and pre-eclampsia (PE)-including defective placentation, maternal vascular malperfusion, and angiogenic imbalance-have been linked to dysregulation of this pathway. During normal gestation, maternal circulating kisspeptin concentrations rise exponentially. In contrast, pregnancies subsequently complicated by FGR or PE, particularly in the early gestation, are associated with reduced levels. However, the comparability of existing studies and their translational applicability are limited by a substantial methodological heterogeneity, including assay variability, gestational age dependence, and inadequate adjustment for maternal confounders. These limitations hinder robust conclusions regarding the role of kisspeptin in placental pathology. This review critically integrates molecular, pathophysiological, and clinical evidence relating to the role of KP-10 in placental dysfunction. The key question is whether KP-10 represents a mechanistic biomarker of trophoblast signalling dysfunction or merely a secondary marker of reduced placental mass; resolving this distinction is essential.

Keywords:  Kisspeptin-10; angiogenesis; angiogenic biomarkers; foetal growth restriction; kisspeptin; kisspeptin receptor; placental dysfunction; pre-eclampsia; spiral artery remodelling; trophoblast invasion

DOI:  https://doi.org/10.3390/ijms27093748
Toxicol Pathol. 2026 May 14. 1926233261439119

Placental Lesions in CD-1 Mouse Placenta Following Gestational Exposure to Perfluorooctanoic Acid (PFOA) or Hexafluoropropylene Oxide Dimer Acid (HFPO-DA or GenX).

Julie F Foley, Catherine A Picut, Vesna A Chappell, Colette N Miller, Suzanne E Fenton, Bevin E Blake.

  Exposure to certain per- and polyfluoroalkyl substances (PFAS) is associated with adverse pregnancy outcomes in mice and humans. These adverse outcomes are suspected to be due to exposure-related toxic effects on the placenta. This study was designed to more explicitly define the effects of selected PFAS on all regions of the placenta of pregnant CD-1 mice. Pregnant CD-1 mice were gavaged with perfluorooctanoic acid (PFOA; 1 or 5 mg/kg-d) or hexafluoropropylene oxide dimer acid (GenX; 2 or 10 mg/kg/day) from embryonic day (E) 1.5 to E17.5. Exposure to either PFOA or GenX resulted in higher placenta weights and lower placental efficiency (embryo:placenta weight ratio). Light microscopic evaluation of the placentae revealed treatment-associated lesions in the decidua, junctional zone, and labyrinth. The reduced placental efficiency and microscopic findings were consistent with maternal vascular malperfusion. With few exceptions, there were no differences between the effects of PFOA when compared with GenX, except for increased necrosis of spongiotrophoblasts in the high-dose PFOA-treated group. Taken together, these findings suggest both PFOA and GenX cause multiple pathological changes at the microscopic and tissue level of the placenta consistent with adverse maternal-fetal health outcomes.

Keywords:  adverse pregnancy outcome; maternal vascular malperfusion; maternal-fetal health; mouse placenta; perfluoroalkyl substance (PFAS); placental pathology

DOI:  https://doi.org/10.1177/01926233261439119
Placenta. 2026 May 13. pii: S0143-4004(26)00176-1. [Epub ahead of print]

Recent innovations in placental MRI: Integrating visualization and functional imaging.

Esra Abaci Turk, Borjan Gagoski, Polina Golland, P Ellen Grant.

  The placenta is a highly specialized organ that regulates oxygen, nutrient, and waste exchange between the maternal and fetal circulations and is essential for normal fetal development and pregnancy outcome. Placental dysfunction underlies many obstetric complications, including fetal growth restriction, pre-eclampsia, congenital heart disease, and stillbirth, yet in vivo assessment of placental structure and function remains limited in routine clinical care. Magnetic resonance imaging (MRI) has emerged as a powerful, noninvasive modality for placental evaluation, offering whole-organ coverage, superior soft-tissue contrast, and the ability to interrogate placental morphology, microstructure, perfusion, and oxygenation across gestation. This review summarizes recent advances in structural, microstructural, and functional placental MRI, with emphasis on quantitative and multimodal approaches. Emerging integrated and multicontrast frameworks that capture placental spatiotemporal heterogeneity and disentangle maternal, fetal, and tissue compartments are highlighted. Finally, we address key technical challenges, including physiological confounders. Continued methodological advancement and large longitudinal studies are essential to translate placental MRI into clinically robust measures of placental health.

Keywords:  Functional MRI; MRI; Placenta; Quantitative MRI; Structural MRI

DOI:  https://doi.org/10.1016/j.placenta.2026.05.014
Bio Protoc. 2026 May 05. 16(9): e5667

Assessing Mitochondrial Respiratory Complex-Associated Function From Previously Frozen Mouse Placental Tissue.

Tina Podinic, Donald Xhuti, Cristina Monaco, Joshua P Nederveen, Sandeep Raha.

  The placenta is a metabolically active organ whose mitochondrial activity is tightly linked to fetal growth, oxygenation, and nutrient transport, mediating fetal susceptibility to environmental exposures. Accordingly, aberrant mitochondrial function has been implicated in the progression of placental dysfunction. However, existing respirometry platforms require primarily fresh or cryopreserved placental tissue and offer limited throughput, rendering these platforms impractical in the context of large-scale placental dissections. Here, we describe and validate a Seahorse XF approach for measuring mitochondrial respiration in previously frozen placentae, enabling the functional interrogation of placental mitochondria in prenatal studies. Our protocol fundamentally relies on the restoration of matrix substrates that are depleted due to increased mitochondrial membrane permeability following freeze-thaw cycles. We provide a strategy to assess complex I and II-associated respiration adapted for the Seahorse XFe24 Analyzer and further demonstrate comparable oxygen consumption readouts between fresh and frozen placentae. We further demonstrate distinct differences in the magnitude of oxygen consumption between fresh and frozen placentae in the absence of exogenous NADH. Taken together, we present a simplified and convenient protocol for the assessment of respiratory enzyme complex-associated respiration from archived placental tissue. Key features • This protocol is suitable for use with previously frozen mouse placental tissue. • Streamlined protocol for complex-associated respirometry assessments following large-scale placental dissections. • Respirometry data may be acquired in <4 hours.

Keywords:  Bioenergetics; Electron transport-chain enzyme activity; Fresh tissue; Frozen tissue; Metabolism; Mitochondria; Oxygen consumption; Placenta; Respiration; Respirometry

DOI:  https://doi.org/10.21769/BioProtoc.5667
Toxicol Pathol. 2026 May 15. 1926233261436343

Select Histochemical and Immunohistochemical Methods to Investigate the Cell and Tissue Composition of the Mouse Placenta and Metrial Gland.

Susan A Elmore, Robert Z Cochran, Charan Ganta, Heather Jensen, Beth A Lubeck, Beth Mahler, David Sabio, Greg Stamper, Brad Bolon.

  Mice as model organisms play a vital role in translational research for developmental biology by aiding our understanding of embryonic and placental evolution in health and various disease states. The close similarity between mouse and human placentas is a great asset in reproductive translational research, making the mouse one of the more prominent model organisms in this field. Mice are routinely used to investigate mechanisms of embryonic and placental development, often through experimental manipulations involving engineered or spontaneous genetic mutations and/or xenobiotic treatments. A crucial aspect of fully appreciating the mouse as a model organism for placental research is understanding the anatomy and physiology of the major embryonic (chorion, labyrinth, junctional zone, and yolk sac) and maternal (decidua basalis and metrial gland) placenta components, including knowledge of the specific cell types active during each gestational stage. This paper discusses histochemical and immunohistochemical (IHC) methods that highlight specific tissue layers and cell types present during normal development of the mouse placenta and maternal metrial gland. Altered numbers and/or locations of these common cell types have been demonstrated in embryonic lethal phenotypes, indicating that placental assessments must examine not only the tissue organization but also affected cell populations when determining the cause of early pregnancy loss.

Keywords:  CK18; IBA1; Ki67; PECAM-1; metrial gland; perforin; placenta

DOI:  https://doi.org/10.1177/01926233261436343
Int J Tryptophan Res. 2026 ;19 11786469261449491

Tryptophan's Journey Through Pregnancy: The Role of Serotonin.

Benoît Gendrot, Cathy Vaillancourt, Guillemette Fouquet.

  Tryptophan is an essential amino acid required for protein synthesis and a precursor of key bioactive metabolites produced through the kynurenine, indole and serotonin pathways. Beyond its nutritional role, tryptophan metabolism critically regulates the nervous, immune and endocrine systems, coordinates circadian rhythms via melatonin, and exerts antioxidant effects. These processes are profoundly remodeled during pregnancy. Pregnancy represents a unique physiological state characterized by systemic adaptations, including changes in immunity and erythropoiesis, while the placenta emerges as a central organ coordinating fetal development, maternal-fetal exchanges, immune tolerance, and protection against external infections. Increasing evidence indicates that tryptophan availability and its downstream metabolites play key roles in maintaining maternal-fetal and placental homeostasis. In particular, serotonin, traditionally viewed as a neurotransmitter, has emerged as a locally produced signaling molecule in the placenta, impacting trophoblast development, placental vascularization, and immune modulation. Dysregulation of tryptophan metabolic pathways has been associated with pregnancy complications and adverse developmental outcomes. This review aims to provide an overview of tryptophan metabolism during gestation, with a specific focus on serotonin as a key factor in placental homeostasis. Targeting tryptophan-derived pathways may offer novel opportunities to improve maternal and neonatal health.

Keywords:  5-HT; embryo; indole; kynurenine; melatonin; placenta

DOI:  https://doi.org/10.1177/11786469261449491
Mol Hum Reprod. 2026 May 13. pii: gaag026. [Epub ahead of print]

Beyond Neurobiology: Cellular Prion Protein (PRNP) as an Emerging Regulator of Decidual and Utero-Placental Vascular Function.

Rumela Bose Banerjee, Rupasri Ain.

  The establishment of a functional utero-placental interface depends on the precise temporal and spatial coordination of blastocyst attachment, decidual transformation, trophoblast invasion, and uterine spiral artery remodelling (SAR). Disruption of these tightly regulated processes underlies major placental pathologies, including preeclampsia, fetal growth restriction, and stillbirth. Although significant advances have been made in defining the molecular networks governing placental development, the contribution of cellular prion protein (PRNP) remains poorly characterized. warranting a focused review. Classically studied in the context of neurobiology and prion-associated neurodegenerative diseases, PRNP is now emerging as an important regulator of reproductive and vascular physiology. This review provides an overview of current evidence supporting non-neuronal roles of PRNP during early pregnancy, with particular emphasis on decidualization and utero-placental vascular adaptation. PRNP displays dynamic expression in the uterine glands, decidua, and vascular smooth muscle cells (VSMCs), where it contributes to tight-junction integrity, decidual cell survival, and autophagic homeostasis. Within the vascular compartment, PRNP regulates trophoblast-directed VSMC phenotypic switching by limiting proliferation, promoting platelet-derived growth factor-β-focal adhesion kinase (PDGFR-β-FAK) -dependent migration, and protecting VSMCs from TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, processes essential for effective SAR. Notably, PRNP expression is transcriptionally regulated by odd-skipped related 1 (OSR1), which is itself negatively modulated by trophoblast cells. Collectively, these findings position PRNP beyond its traditional neurobiological role as a sensitive molecular indicator of decidual competence and vascular remodelling status, highlighting its potential as a biomarker and therapeutic target in placental disorders.

Keywords:  Apoptosis; Autophagy; Migration; Phenotypic switching; Spiral artery remodelling; Trophoblast; Vascular Smooth Muscle cells

DOI:  https://doi.org/10.1093/molehr/gaag026
Nat Commun. 2026 May 13.

Defective O-fucosylation of EDIL3 attenuates invasion and vascular remodeling of trophoblasts via LIFR signaling pathway in preeclampsia.

Yaqi Li, Hongpan Wu, Yuyu Lei, Shuyu Bai, Jiao Wang, Bin Yan, Yubo Liu, Shuai Liu.

Preeclampsia (PE) is a severe pregnancy disorder caused by placental dysfunction. Protein O-fucosylation is a type of protein post translational modification that is catalyzed by protein O-fucosyltransferases (poFUTs). However, the role and underlying mechanisms of O-fucosylation/poFUT1 in PE remain elusive. Here, we revealed a lower level of poFUT1 in the plasma and placental tissues of PE patients than in normal pregnancy (NP) women. Moreover, poFUT1 deletion induced PE-like phenotypes in a mouse model. Mechanistically, we globally screened O-fucosylated proteins and identified EDIL3 with an O-fucosylation site at threonine 88. Furthermore, O-fucosylation-EDIL3 can directly interact with LIFR on trophoblasts, consequently activating the STAT3 signaling pathway, promoting the invasion and vascular remodeling ability of trophoblasts. Conversely, de-O-fucosylation-EDIL3 aggravated PE-like phenotypes by attenuating placental development in vitro and in vivo. Our data elucidate the function of poFUT1/O-fucosylation EDIL3/LIFR axis during placental development, providing glycol-based target for diagnostic and therapeutic of preeclampsia.

DOI: https://doi.org/10.1038/s41467-026-73139-4
Placenta. 2026 May 13. pii: S0143-4004(26)00173-6. [Epub ahead of print]181 102-107

Clearing for insight: A light-sheet microscopy workflow for 3D vascular reconstruction in human first trimester placental villi and decidua.

Désirée Forstner, Christine Daxböck, Monika Siwetz, Stefan Wernitznig, Selina J Keppler, Katja Sallinger, Michael Gruber, Daniel Kummer, Thomas Kroneis, Berthold Huppertz, Martin Gauster.

  The 3D visualization of the maternal-fetal interface is essential for understanding human placental development, yet remains technically challenging due to tissue opacity and structural complexity. Here, we describe a robust light-sheet fluorescence microscopy workflow optimized for imaging first-trimester placental villi and decidua, which were cleared, multiplex immunofluorescence labeled, and imaged by light-sheet microscopy. Pan-cytokeratin, CD31 or CD34, and alpha smooth muscle actin staining enabled 3D reconstruction of the vascular architecture in placental villi and decidua parietalis. This workflow may aid in elevating previous 2D observations into a 3D context, offering a more comprehensive view of tissue organization at the early maternal-fetal interface.

Keywords:  3D reconstruction; Decidua; Human first trimester placenta; Light-sheet fluorescence microscopy; Placental villi; Vasculature

DOI:  https://doi.org/10.1016/j.placenta.2026.05.011
Biol Reprod. 2026 May 14. pii: ioag103. [Epub ahead of print]

Disturbances of the Placenta-Brain Axis in Germ-Free Pregnant Mice.

Rosalind T B Herrington, Zhen Lyu, Ragavi Raman, Sarah E Seda, Claire Snyder, Nathan J Bivens, Zhentian Lei, Tanhaul Islam, Lloyd W Sumner, Trupti Joshi, Cheryl S Rosenfeld.

  Maternal gut microbiota changes can profoundly shape on offspring health. The placenta may be vulnerable to maternal gut microbiota alterations. Placental disruptions can influence fetal brain development and underly risks for neurobehavioral disorders. Maternal gut microbiota disruptions might affect the placenta through alterations in bacterial short chain fatty acids (SCFA). The hypothesis tested is that depletion of maternal gut microbiota, as may occur in pregnant women treated with antibiotics and germ-free (GF) mice, impacts bacterial SCFA in her fecal samples and in placenta and fetal brain. We assessed whether transcriptomic changes would be evident in placenta and fetal brain from conceptuses derived from GF relative to multi-pathogen free (MPF) pregnant females. Maternal GF status reduced the concentrations of all measured SCFA within the stool. Surprisingly, two-methylbutanoic acid was significantly increased in male and female placenta and fetal brain samples in conceptuses from GF dams. In female and male placenta, several Prl form had altered expression in conceptuses from GF dams. In male placenta from GF dams, Hsd11b2 and Dio3 showed increased expression. Decreased expression of Sl6a2 and Slc22a3 in female fetal brain from GF dams might influence uptake of catecholamines. Results reveal depletion of maternal microbiota can lead to striking effects on the placenta-fetal brain axis. Findings raise concern as to whether maternal microbiota alterations due to other intrinsic or extrinsic factors, namely antibiotic treatment, might impact transcriptomic profiles in fetal placenta and brain. Underlying mechanisms remain uncertain but may relate to changes bacterial metabolites transferred from mother to conceptus.

Keywords:  Gut Microbiome; Metabolomics; Pregnancy; Short-Chain Fatty Acids; Transcriptomics; Trophoblast

DOI:  https://doi.org/10.1093/biolre/ioag103
Mol Hum Reprod. 2026 May 12. pii: gaag030. [Epub ahead of print]

Stem Cell-based Embryo Models as a tool for reproductive biology.

Alfonso Martinez Arias, Andre Dias, Maneesha Inamdar.

  ART has transformed clinical practice but still face modest success rates, poorly defined implantation conditions, and persistent gaps in understanding early human development. At the same time, research in human reproductive biology remains strikingly underfunded relative to its medical and social impact. Over the last decade, advances in human pluripotent stem cell (PSC) biology have generated a suite of technologies that can recapitulate early stages of human development from blastocyst formation to early gastrulation in vitro. Here we review how such models can be harnessed to interrogate lineage specification, embryo-endometrium crosstalk, the origins of aneuploidy and implantation failure, and the developmental basis of placental and yolk sac disorders, with a focus on primates. We argue that integrating stem cell-derived embryo models into reproductive research agendas offers a tractable experimental framework to improve ART outcomes and address major unmet needs in human reproductive health.

Keywords:  Embryology; Gene expression; Implantation; Pregnancy; Stem cells

DOI:  https://doi.org/10.1093/molehr/gaag030
Reproduction. 2026 May 12. pii: xaag058. [Epub ahead of print]

Uterine fluid EV miR-223-3p as endometrial receptivity biomarker and regulator in implantation.

Xi Huang, Aihua He, Runxin Gan, Qiong Zhang, Jing Zhao, Jing Fu, Yanping Li.

  Endometrial receptivity (ER) is a pivotal determinant of successful embryo implantation, yet its regulation by uterine fluid (UF) extracellular vesicles (EVs) remains poorly understood. This study aimed to identify key UF EV miRNAs during the endometrial receptive period and observe the role in implantation. .UF EVs were isolated from the same in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) patients at two time points: the pre-receptive (LH + 3/p + 1) and receptive (LH + 7/p + 5). miRNA sequencing and validation identified miR-223-3p as the key miRNA. Bioinformatic analysis predicted FOXO1 as a primary target, forming a hub genes complex with H3-3B and SIRT1. To investigate the functional role of UF EVs miR_223-3p, EVs with reduced miR-223-3p were isolated from the culture medium of sh-miR-223-3p ishikawa cells. Functional studies demonstrated that after EVs internalization by trophoblast cells, led to a significant reduction in miR-223-3p levels. This knockdown resulted in markedly impaired trophoblast proliferation, migration, invasion, and adhesion. Concurrently, FOXO1 were significantly downregulated. We propose a novel model whereby receptive endometrium selectively packages miR-223-3p into UF EVs, which are then internalized by the embryo to modulate trophoblast function through the FOXO1/H3-3B/SIRT1 complex. UF EV miR-223-3p emerges as a critical regulator of ER and a promising non-invasive biomarker for assessing implantation competence.

Keywords:  extracellular vesicle; implantation; miR-223-3p; uterine fluid

DOI:  https://doi.org/10.1093/reprod/xaag058
Nat Commun. 2026 May 12.

Conserved pathogenesis of ancestral and contemporary Oropouche virus strains in a murine pregnancy model.

Krista B Gunter, James M Bowen, Andrew T Clarke, Melanie McFarlane, Dorcus C A Omoga, Stephanie Pozuelos, Henry Giesel, Curtis Witt, Lisa M Rogers, David M Aronoff, Andrew M Lunel, Jay Vornhagen, Benjamin Brennan, Natasha L Tilston.

Oropouche virus (OROV) is an emerging orthobunyavirus responsible for widespread outbreaks across South and Central America. Recent reports of congenital disease have raised urgent concerns regarding the potential risk of OROV infection during pregnancy. Here, we establish an in vivo murine model of OROV vertical transmission using the ancestral (prototype) strain BeAn19991 in immunocompetent C57BL/6 J mice. We demonstrate that OROV robustly replicates in maternal tissues and efficiently infects the placenta. Complementary studies in human trophoblast-derived cell lines demonstrate conserved placental tropism across both the ancestral strain and a contemporary (outbreak) isolate, supporting the translational relevance of our findings. Notably, comparison of ancestral and contemporary viruses indicates that placental infection is not a recently acquired property of OROV. Further, offspring born to infected dams exhibit maternally derived neutralizing antibodies and transient protection upon postnatal challenge. Together, these findings, considered alongside emerging epidemiological evidence, identify pregnancy as a critical context for OROV infection and underscore the need to evaluate risks to pregnant individuals in endemic regions.

DOI: https://doi.org/10.1038/s41467-026-72711-2
J Obstet Gynaecol Can. 2026 May 12. pii: S1701-2163(26)00195-7. [Epub ahead of print] 103393

Clinical Considerations for Implementing Placental Growth Factor-based testing in Urban and Rural regions in Canada.

Jessica Liauw, Jennifer A Hutcheon, Elise Lavoie Lebel, Karen C Tran.

  Placental growth factor (PlGF)-based testing is a promising strategy to improve risk stratification of pregnant individuals presenting with hypertensive disorders of pregnancy in Canada. However, implementation of PlGF-based testing may have different implications in urban versus rural regions. In this review we summarize key evidence on PlGF-based testing for individuals with suspected or confirmed preeclampsia and describe differences in how it may translate to urban and rural practice settings. We use clinical vignettes to illustrate practical impacts and challenges of using PlGF-based testing for a typical clinical scenario presenting to Canadian centres.

Keywords:  Placenta Growth Factor; Pre-Eclampsia; Risk Assessment

DOI:  https://doi.org/10.1016/j.jogc.2026.103393