bims-placeb Biomed News
on Placental cell biology
Issue of 2026–03–29
twelve papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences



  1. bioRxiv. 2026 Mar 17. pii: 2026.03.14.711150. [Epub ahead of print]
      Differentiation of trophoblast stem (TS) cells or progenitor cytotrophoblasts (CTBs) into multinucleated syncytiotrophoblasts (STBs) is essential for placental development. Disruption of this process contributes to major obstetrical syndromes, including fetal growth restriction and preeclampsia, and Trisomy 21. However, the chromatin mechanisms governing trophoblast stemness and differentiation remain inadequately defined. Here we identify the chromatin-associated factor PHF13, uncovered through a high-throughput microRNA target screen, as a key regulator of trophoblast cell fate. PHF13 knockout TS cells exhibited defects that ultimately resulted in loss of cell viability, whereas PHF13 knockdown promoted expression of fusion-associated genes, including ERVFRD-1 and human chorionic gonadotropin (hCG). Consistently, PHF13 depletion in BeWo trophoblast cells increased hCG expression and secretion while reducing expression of canonical stemness-associated transcription factors ELF5 and TEAD4. Integrated genomic analyses further revealed that PHF13 target genes comprise a gene regulatory network that maintains trophoblast stemness and restrains differentiation. Notably, the pluripotency-associated transcription factor THAP11 partially co-occupies genomic sites with PHF13. Together, these findings establish PHF13 as a previously unrecognized chromatin regulator of trophoblast stemness and differentiation, providing mechanistic insight into pathways critical for placental development and function.
    DOI:  https://doi.org/10.64898/2026.03.14.711150
  2. Biomolecules. 2026 Mar 03. pii: 383. [Epub ahead of print]16(3):
      Three-dimensional (3D) organoid and co-culture models have emerged as transformative tools for studying human endometrial function, implantation, and placental development, overcoming key limitations of animal and two-dimensional in vitro systems. This review synthesises available information of recent advances in endometrial epithelial organoids (EEOs), trophoblast organoids (TBOs), and increasingly complex co-culture platforms incorporating stromal, vascular, and trophoblast compartments to model epithelial-stromal crosstalk, decidualisation, angiogenesis, and embryo implantation. Emerging developments include assembloid systems, synthetic and semi-synthetic extracellular matrices, and microfluidic organ-on-a-chip technologies that enable long-term culture, hormonal responsiveness, and patient-specific modelling. These approaches have recapitulated key features of the mid-secretory endometrium, placental villous architecture, trophoblast differentiation, and early implantation events while revealing disease-associated dysfunctions in conditions such as endometriosis, adenomyosis, polycystic ovarian syndrome, and endometrial cancer. Despite significant progress, current models remain limited by incomplete cellular diversity, polarity constraints, and challenges in fully modelling immune and vascular interactions. Collectively, emerging 3D organoid and co-culture systems provide physiologically relevant platforms to interrogate human reproductive biology, elucidate mechanisms underlying implantation failure and placental disease, and support the development of personalised therapeutic strategies to improve reproductive outcomes.
    Keywords:  embryo implantation; endometrial epithelial organoids; endometrium; placenta; trophoblast organoids; uterus
    DOI:  https://doi.org/10.3390/biom16030383
  3. Cell Death Dis. 2026 Mar 26.
      Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is a leading cause of maternal and perinatal morbidity and mortality. Its early-onset form (EO-PE), requiring delivery before 34 weeks of gestation, is particularly severe and closely linked to defective trophoblast differentiation. Here, we identify BRCA1-associated protein 1 (BAP1) and its cofactors ASXL2 and ASXL3 as upregulated in EO-PE placentas. Enforced BAP1 expression in human trophoblast stem cells reinforced epithelial identity, enhanced adhesion, and impaired both extravillous trophoblast differentiation and syncytiotrophoblast formation. Integrated transcriptomic and proteomic analyses revealed suppression of lineage-specific pathways alongside maintenance of progenitor-like and pro-inflammatory signatures. In trophoblast organoids, an excess of BAP1 disrupted syncytial maturation and induced interferon-driven pathways overlapping with EO-PE transcriptomes. Together, these findings establish BAP1 as a key regulator of human trophoblast differentiation and implicate its dysregulation in the pathogenesis of EO-PE, providing mechanistic insight into the cellular basis of placental dysfunction.
    DOI:  https://doi.org/10.1038/s41419-026-08650-z
  4. Biomolecules. 2026 03 15. pii: 441. [Epub ahead of print]16(3):
      A revised two-stage model of preeclampsia is proposed, centering on an autophagy-dependent requirement for extravillous trophoblast entry into the proximal one-third of the myometrium. The One-Third Myometrium Enigma, introduced here, denotes the unresolved physiological rule that early placentation requires trophoblasts to traverse decidua and reach the proximal one-third of myometrium under hypoxia and nutrient scarcity. The hypothesis posits a timed rise in basal autophagy to sustain trophoblast energy homeostasis and invasion, accompanied by TFEB-driven lysosomal programs that enable villous cytotrophoblast syncytialization. Autophagic dysfunction could contribute to shallow invasion, chronic placental hypoxia, fetal growth restriction, and release of placental injury signals preceding maternal syndrome. Potential failure modes include reduced autophagic flux due to inhibition of autophagosome to lysosome fusion or mistimed persistence of hypoxia signaling, such as prolonged HIF-1α activity. Collectively, this evidence suggests that impaired autophagy is a testable contributor to preeclampsia pathogenesis. Predictions include early risk stratification with circulating autophagy markers and extracellular vesicle microRNAs, and therapeutic benefit from autophagy modulation that targets AMPK or mTOR or activates TFEB with safety constraints. This framework reframes preeclampsia as a disorder of placental quality control and specifies where and when autophagy may be required.
    Keywords:  TFEB; autophagy; preeclampsia
    DOI:  https://doi.org/10.3390/biom16030441
  5. iScience. 2026 Apr 17. 29(4): 115205
      The placenta is vital for fetal development, and altered placental vascularization, the most common placental pathology, underlies prevalent disorders, including fetal growth restriction, prematurity, and pregnancy complications. Impaired placental vascularization is associated with Vitamin A deficiency, but the mechanisms are undefined. To investigate this, we used retinoic acid (RA)-deficient Raldh2-/- embryos, and found they exhibit allantoic and placental endothelial hyperproliferation and impaired arterial-venous remodeling, which were rescued by providing all-trans-RA (ATRA) via maternal diet. Single-cell RNA sequencing of E9.5 Raldh2 +/+ , Raldh2-/-, and Raldh2-/- + ATRA placental cells, and functional assays, revealed that RA regulates endothelial growth and vascular remodeling via Notch signaling. We also uncovered a PLEXIND1-SEMA3E/F signaling axis between fetal endothelial cells and chorionic trophoblast precursors that is impaired with RA deficiency and rescued with ATRA. Our data suggest that RA-mediated signaling regulates allantois and placental endothelial cell growth, specification, and guidance required for chorioallantoic fusion and fetoplacental vascularization.
    Keywords:  cell biology; developmental biology; molecular biology
    DOI:  https://doi.org/10.1016/j.isci.2026.115205
  6. Clin Sci (Lond). 2026 Mar 25. pii: CS20257407. [Epub ahead of print]
      SARS-CoV-2 infection disrupts iron homeostasis in organs such as the lung. Emerging evidence suggests similar dysregulation in the placenta may impair function and fetal growth. Ferroptosis, an iron-dependent form of cell death is driven by the accumulation of ferrous labile iron, catalyzing the peroxidation of polyunsaturated fatty acids in the absence of sufficient iron storage or antioxidant defenses. This pathway has been implicated in SARS-CoV-2-related tissue damage in other organs and may contribute to placental dysfunction during pregnancy. However, the influence of infection timing, symptom severity, and fetal sex on placental iron regulation remains unexamined. We analyzed placental samples from a cohort of SARS-CoV-2 exposed pregnancies in the first (n=6), second (n=14) or third trimester (n=30), classified by symptom severity (asymptomatic n=23, symptomatic n=27) and fetal sex, alongside unexposed controls (n = 47). We assessed placental iron deposition, lipid peroxidation, mRNA and protein expression of ferroptosis markers. Publicly available RNA-sequencing datasets from human placenta tissue, exposed or not to SARS-CoV-2, were analyzed to assess ferroptosis-related genes expression. SARS-CoV-2-infection, particularly in symptomatic cases, was associated with reduced placental weight and birthweight. Asymptomatic cases showed increased placental iron deposition, which correlated with lower birthweight and was accompanied by elevated expression of Nuclear Receptor Coactivator 4 (NCOA4), a cytosolic adaptor protein that mediates the selective autophagic degradation of ferritin (ferritinophagy) and iron release. Placentas from symptomatic patients exhibited evidence of altered iron transport and sex-specific downregulation of antioxidant defenses. Transcriptomic analyses further suggested widespread disruption of ferroptosis pathways in placentas from infected patients. Our findings reveal that SARS-CoV-2 infection alters placental iron homeostasis and is associated with ferroptosis-related changes, with distinct molecular responses based on timing of infection, symptom severity and fetal sex.
    Keywords:  COVID-19; Ferritinophagy; Ferroptosis; Iron metabolism; Placenta; SARS-CoV-2
    DOI:  https://doi.org/10.1042/CS20257407
  7. EMBO Mol Med. 2026 Mar 24.
      Air particulate matter (PM2.5 and PM10), can cross the placental barrier, triggering oxidative stress and inflammation that compromise fetal development. These insults lead to placental dysfunction and complications including preterm birth, low birth weight, and preeclampsia. In cell line and placental explant models, urban particulate matter (UPM) increased pro-inflammatory cytokines and oxidative stress pathways, impairing trophoblast invasion, angiogenesis, and nutrient transport, while also altering epigenetic modifications and endoplasmic reticulum function. Rodent studies revealed reduced litter size, placental abnormalities, and fetal growth arrest along with postnatal neurodevelopmental alterations. Human cohorts from high-exposure regions showed elevated low birth weight rates. Proteomic and transcriptomic analyses of rat placenta revealed an inflammatory signature and altered metabolic networks, while gut microbiome dysbiosis suggested links to metabolic disturbances. Importantly, transcriptomic analysis identified IGFBP3 as a major downregulated gene following UPM exposure. IGFBP3, a key regulator of IGF bioavailability, was suppressed by IL1β, establishing inflammation-driven repression as the mechanism. These findings underscore UPM's multidimensional impact on maternal-fetal health and highlight preventive strategies as urgent priorities.
    Keywords:  Fetal Neurodevelopment; Inflammation; Insulin-like Growth Factor Binding Protein 3 (IGFBP3); Trophoblast differentiation; Urban Particulate Matter
    DOI:  https://doi.org/10.1038/s44321-026-00403-x
  8. Sci Rep. 2026 Mar 25. pii: 8162. [Epub ahead of print]16(1):
      During early pregnancy, many women experience physical changes, including nausea and vomiting of pregnancy (NVP), which negatively impact their quality of life. However, the absence of model animals has limited our understanding of such pregnancy-associated physiological changes. Here, we examined pregnancy-associated metabolic and behavioral changes in common marmosets and mice. Marmosets exhibited a transient weight decrease during the period of placental development in approximately 22% of pregnancies. Some marmosets repeatedly showed transient weight loss across multiple pregnancies, suggesting individual variations in the likelihood of pregnancy-associated weight loss. Although mice did not show apparent alteration in body weight, they exhibited a slowdown in food intake and alterations in locomotor activity during the corresponding phase. The observed transient changes in pregnant marmosets and mice may provide a basis for generating hypotheses regarding physiological changes associated with placentation.
    Keywords:  Common marmoset; Morning sickness; Mouse; Nausea and vomiting of pregnancy
    DOI:  https://doi.org/10.1038/s41598-026-41314-8
  9. Biol Reprod. 2026 Mar 24. pii: ioag066. [Epub ahead of print]
      For a brief but critical period post-fertilization, the mammalian embryo is entirely dependent on maternal products inherited from the oocyte. Previous research showed that oocyte-specific loss of Med12, an X-linked gene and Mediator complex subunit, leads to female sterility despite normal folliculogenesis and ovulation. Here, we show that loss of maternal Med12 has minimal effect on the oocyte transcriptome and does not manifest in embryonic lethality until post-implantation. Implants derived from Med12-null oocytes demonstrate abnormal placentation at E9.5, with an overabundance of trophoblast giant cells (TGC). This phenotype associates with early disruption of lineage markers at the blastocyst stage (e.g. Pou5f1 and Gata3), and later by downregulation of trophoblast pluripotency markers (e.g. Cdx2) and activation of drivers of TGC identity (e.g. Stra13) in the E7.5 extraembryonic ectoderm, revealing a previously undescribed role for Med12 in trophoblast pluripotency maintenance. Notably, we find consistently low Med12 expression in embryos derived from Med12-null oocytes, likely due to programmed paternal X chromosome inactivation (XCI). To isolate the consequences of maternal Med12 depletion, we introduced an autosomal Med12 transgene and show that embryonic expression of the transgene rescues development of Med12-null oocytes. We conclude that oocyte-specific deletion of Med12 produces a maternal-zygotic double knock-out in extraembryonic tissues due to paternal XCI, leading to loss of pluripotency in the trophoblast, placental malformation, and embryonic death.
    Keywords:  Maternal effect gene; Mediator; development; embryonic lethality; placenta; trophoblast
    DOI:  https://doi.org/10.1093/biolre/ioag066
  10. J Matern Fetal Neonatal Med. 2026 Dec;39(1): 2648178
       OBJECTIVE: To review the current role of soluble fms-like tyrosine kinase-1 (sFLT1) and placental growth factor (PlGF) in the pathophysiology, diagnosis, prediction, and treatment of preeclampsia.
    BACKGROUND: Preeclampsia is a major cause of maternal and perinatal morbidity and mortality worldwide and has increased in prevalence in the United States. It is characterized by new-onset hypertension, proteinuria, and/or end-organ dysfunction, with early-onset disease often associated with placental ischemia, placental insufficiency, and fetal growth restriction. A central mechanism in preeclampsia is angiogenic imbalance, characterized by increased antiangiogenic factors, particularly sFLT1, and reduced proangiogenic signaling mediated by VEGF and PlGF.
    METHODS: This review summarizes current evidence regarding sFLT1 biology, the clinical utility of the sFLT1/PlGF ratio, and emerging therapeutic strategies targeting sFLT1 in preeclampsia.
    RESULTS: sFLT1 is a soluble splice variant of VEGF receptor-1 that binds circulating VEGF and PlGF, thereby promoting endothelial dysfunction, vasoconstriction, and systemic manifestations of preeclampsia. The sFLT1/PlGF ratio has emerged as a clinically useful biomarker, particularly for short-term risk stratification in women with suspected preeclampsia, with strong negative predictive value for ruling out progression to severe disease within 1 to 2 weeks in appropriately selected patients. The ratio has been incorporated into clinical practice in multiple countries and was approved by the US Food and Drug Administration in 2023 for inpatient risk assessment in singleton pregnancies between 23 and 34 weeks and 6 days of gestation with hypertensive disorders of pregnancy. In parallel, therapeutic approaches targeting sFLT1, including small interfering RNA, antibodies, VEGF or PlGF-based molecular strategies, and apheresis, have shown promise in preclinical and early translational studies.
    CONCLUSION: sFLT1 is central to the pathophysiology of preeclampsia and has substantial clinical relevance as both a biomarker and a potential therapeutic target. The sFLT1/PlGF ratio is reshaping risk assessment and management of preeclampsia, while sFLT1-directed therapies may offer future disease-modifying treatment options. Further refinement of biomarker-guided use and therapeutic development is needed before broader implementation.
    Keywords:  Hypertensive disorders of pregnancy; greater obstetrical syndrome; placental insufficiency; preeclampsia biomarkers; soluble FMS-like tyrosine kinase-1; vascular endothelial growth factor
    DOI:  https://doi.org/10.1080/14767058.2026.2648178
  11. Pregnancy Hypertens. 2026 Mar 22. pii: S2210-7789(26)00033-4. [Epub ahead of print]44 101446
       OBJECTIVE: Twin gestations have high prevalence of hypertensive disorders of pregnancy (HDP). The underlying placental pathology associated with HDP in twin pregnancies is not well established.
    STUDY DESIGN: This is a retrospective cohort study in a single healthcare system. Patients with diamniotic twin gestation and placental pathology were included. Demographic and clinical information was abstracted.
    MAIN OUTCOME MEASURES: All placentas were evaluated for the presence (in one or both placentas) of four pathologic categories. Among those with HDP, placental pathology was compared by delivery timing of <36 weeks and ≥ 36 weeks. Multivariable logistic regression was utilized to assess the independent association of placental histology in HDP vs no HDP and subsequently among those with HDP by early (<36 weeks) vs late (≥36 weeks) delivery.
    RESULTS: A total of 456 patients were included, 151 of which had HDP (33%). Pregnancies with HDP had CI in 35.1%, MVM in 36.4%, FVM in 36.4% and AI in 24.5%. There was increased MVM among those with HDP (aOR MVM 1.60 95% CI 1.03, 2.46). Among pregnancies with HDP, MVM was increased at <36 weeks vs ≥ 36 weeks (56.1% vs 24.5%, aOR 4.80 (95% CI 2.23, 10.35) p < 0.011), whereas CI was less common (aOR 0.27, 95% CI 0.12, 0.63, p < 0.01).
    CONCLUSION: MVM is more common in HDP, especially in those delivering <33 weeks than at term, and CI is more common in HDP delivering at term. Further work is needed in understanding the pathophysiology of HDP in twin gestation.
    Keywords:  Hypertensive disorder of pregnancy; Multiple gestation; Placental pathology
    DOI:  https://doi.org/10.1016/j.preghy.2026.101446
  12. Mol Reprod Dev. 2026 Mar;93(3): e70100
      Heat stress impairs the reproductive capacity of organisms. In contrast, thermal adaptation can have beneficial effects. In this study, we investigated the mechanism through which thermal adaptation (39°C for 1 h followed by recovery at 37°C for 3 h) improves the quality of in vitro cultured mouse morula-stage embryos. Thermal adaptation resulted in several key changes: increased expression of genes associated with embryo quality (Cdh1, Gja1, Dnmt1); decreased expression of Wnt and mTOR genes and proteins; and upregulated expression of GSK3β and autophagy-related markers (LC3B, Beclin-1). Consequently, thermal adaptation increased the blastocyst rate and improved embryo quality. These findings suggest that thermal adaptation during early embryo development enhances developmental competence by inhibiting the Wnt signaling pathway and activating autophagy.
    Keywords:  Wnt signaling pathway; autophagy; mouse morula; thermal adaptation
    DOI:  https://doi.org/10.1002/mrd.70100