bims-placeb Biomed News
on Placental cell biology
Issue of 2026–06–21
seven papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences
  1. Maternal microRNAs linked to birth deficits due to prenatal alcohol exposure are dominant modifiers of gene expression in invasive trophoblast cells.
  2. The SIRT1-p53 axis drives a ferro-aging-like program and aggravates trophoblast dysfunction in preeclampsia.
  3. Placental Dysfunction in Cloned Pigs Linked to Impaired Trophoblast Adhesion and Vascular Development.
  4. PLACENTAL AND FETAL RESPONSES TO ADRENOMEDULLIN DEFICIENCY IN THE RAT.
  5. Fetoplacental microcirculation abnormalities are reversed by aerobic exercise in mice with preeclampsia.
  6. The placenta as the missing link in pregnancy after metabolic bariatric surgery.
  7. The Old Lady spider cave skeletons in Ladakh have diverse maternal genetic origin.
  1. Front Cell Dev Biol. 2026 ;14 1834760
    Maternal microRNAs linked to birth deficits due to prenatal alcohol exposure are dominant modifiers of gene expression in invasive trophoblast cells.
    Deepa Upreti, Christina D Chambers, Rajesh C Miranda.
       Introduction: Prenatal alcohol exposure (PAE) can impair placental development and result in fetal growth restriction. However, the underlying molecular mechanisms are unclear. We previously found that PAE in some, but not all pregnancies, resulted in significantly elevated circulating levels of 11 microRNAs (HEamiRNAs) in the 2nd trimester. This subgroup of PAE women experienced adverse infant birth outcomes due to PAE, Subsequently, these HEamiRNAs collectively but not individually, were found to inhibit a defined set of placental epithelial-mesenchymal transition (EMT) genes and, inhibited invasiveness of placental trophoblast cells.
    Methods: Here we extend these findings by performing whole-transcriptome analysis to dissect the contribution of ethanol compared to HEamiRNAs in HTR-8/SVneo cells, a model for invasive, human extravillous trophoblasts.
    Results: We observed a large, distinct and statistically greater effect of HEamiRNAs mimics on trophoblast transcript profiles irrespective of ethanol exposure, specifically on EMT, extracellular matrix, angiogenesis and immune signaling pathways among others. Weighted gene co-expression network analysis (WGCNA) identified additional placental growth networks related to epithelial cell proliferation and differentiation and MAPK/PI3K, Hippo and Rap1 signaling.
    Discussion: This study provides a mechanistic framework to explain that the effects of PAE vary across pregnancies, because they are contingent in part, on the elevation key maternal circulating miRNAs.
    Keywords:  fetal growth restriction; miRNAs; placenta; prenatal alcohol exposure; transcriptional regulation
    DOI:  https://doi.org/10.3389/fcell.2026.1834760
  2. Front Aging. 2026 ;7 1838730
    The SIRT1-p53 axis drives a ferro-aging-like program and aggravates trophoblast dysfunction in preeclampsia.
    Rong Hu, Zhi Chen, Wei Bian, Jing Zhang, Xiaoqin Xu, Hui Xiong, Shaojian Xiang, Yubin Ding, Hongbo Qi, Huan Yang.
      Preeclampsia (PE) is a pregnancy-specific syndrome driven by placental dysfunction, and premature placental senescence has increasingly been implicated in its pathogenesis. However, the upstream regulatory mechanisms remain poorly understood. Here, we found that placental SIRT1 expression was reduced in PE and was accompanied by senescence-associated features. In trophoblasts, SIRT1 knockdown enhanced senescence and senescence-associated secretory phenotype (SASP) release, while impairing proliferative capacity, migration, and invasion, whereas pharmacological activation of SIRT1 attenuated placental senescence and ameliorated PE-like manifestations in vivo. Mechanistically, iron chelation alleviated senescence, whereas senolytic intervention partially restored iron homeostasis, supporting a self-reinforcing interaction between iron dyshomeostasis and senescence. Collectively, these findings identify the SIRT1-p53 axis as an upstream regulator linking iron dyshomeostasis to placental senescence, support the existence of a ferro-aging-like pathogenic program in diseased placentas, and provide new insights into the molecular basis of placental dysfunction in PE.
    Keywords:  SIRT1; ferro-aging-like; iron dyshomeostasis; preeclampsia; premature placental senescence; trophoblast dysfunction
    DOI:  https://doi.org/10.3389/fragi.2026.1838730
  3. Mol Reprod Dev. 2026 Jun;93(6): e70122
    Placental Dysfunction in Cloned Pigs Linked to Impaired Trophoblast Adhesion and Vascular Development.
    Xia Zhang, Xin Liu, Cheng-Li Dou, Xiao-Li Liu, Tian Xu, Weiwei Wang, Jingjing Zhang, Hainan He, Linhui Wu, Mei Yu, Yi-Liang Miao.
      Animal cloning, while promising for livestock breeding and genetic improvement, is hampered by low efficiency largely due to placental abnormalities. This study investigated this issue in cloned pigs at the 35th day of gestation, where a 69.8% developmental abnormality rate was observed. Morphological analyses revealed structural defects in placentas from failed pregnancies, including delayed fold development and abnormal areolae formation, coupled with reduced endometrial glands and maternal-side blood vessels. Immunohistochemistry demonstrated impaired placental function, evidenced by aberrant E-cadherin expression compromising trophoblast adhesion, and significantly reduced glycogen/polysaccharide secretion. Furthermore, Plet1 expression was disrupted. Transcriptomic profiling indicated that upregulated genes were enriched in cell-cell tight junctions, while downregulated genes were associated with oxygen binding, oxidative stress, stromal differentiation, and vascular development. Cross-species comparison with cloned mice suggested conserved genetic mechanisms underlying placental defects. These findings provide a crucial theoretical foundation for elucidating the mechanisms of placental failure in animal cloning and for developing strategies to enhance its efficiency.
    DOI:  https://doi.org/10.1002/mrd.70122
  4. Biol Reprod. 2026 Jun 16. pii: ioag125. [Epub ahead of print]
    PLACENTAL AND FETAL RESPONSES TO ADRENOMEDULLIN DEFICIENCY IN THE RAT.
    Marija Kuna, Khursheed Iqbal, Kelly Gorman, Laszlo Balint, Keisuke Kozai, Masanaga Muto, Ayelen Moreno-Irusta, Marc Parrish, Kathleen M Caron, Michael J Soares.
      Adrenomedullin (ADM) is a peptide hormone with a broad spectrum of actions on vascular smooth muscle, endothelial cells, and immune cells. These ADM cellular targets are prominent constituents of the uterine-placental interface that undergo structural and functional transformation during pregnancy. To explore the biology of ADM at the uterine-placental interface, we examined ADM expression using in situ hybridization and generated and characterized an ADM mutant rat model using CRISPR-Cas9-mediated genome editing. At midgestation, Adm was prominently expressed in trophoblast giant cells. Adm expression shifted to the mesometrial uterus as gestation progressed. A germline Adm mutant model was generated. Adm heterozygous males and females were fertile; however, Adm heterozygous intercrosses did not generate live Adm null rats. Adm null fetal-placental sites were viable until gestation day (gd) 15.5. Viable null fetuses were not identified after gd 15.5. Fetal and placental growth restriction were evident on gd 13.5. On gd 15.5 some Adm null placentas exhibited prominent hemorrhagic regions, whereas both hemorrhage and edema were evident in gd 15.5 Adm null fetuses. Our results indicate that ADM serves as a regulator of placental and fetal development.
    Keywords:  adrenomedullin; fetal heart; fetal lymphatic vessels; placenta; trophoblast cells
    DOI:  https://doi.org/10.1093/biolre/ioag125
  5. J Appl Physiol (1985). 2026 Jun 15.
    Fetoplacental microcirculation abnormalities are reversed by aerobic exercise in mice with preeclampsia.
    Daniella Leal Lamarca Bomfim, Fábio das Índias Dos Santos Carvalho, Karine Lino Rodrigues, Evelyn Nunes Goulart da Silva Pereira, Beatriz Peres de Araujo, Raquel Rangel Silvares, Elen Mello de Souza, Caroline Fernandes-Santos, Anissa Daliry.
      Preeclampsia (PE) is a hypertensive disorder of pregnancy characterized by hypertension and organ dysfunction, and is associated with impaired placental perfusion and systemic endothelial dysfunction. Aerobic exercise has been proposed as a potential non-pharmacological strategy to improve vascular function during pregnancy; however, its effects on fetoplacental microcirculation in PE remain poorly understood. Therefore, the objective of this study was to investigate whether maternal aerobic exercise during gestation could influence fetoplacental perfusion and maternal pathological features in an experimental model of PE induced by nitric oxide synthase inhibition. Fetoplacental and fetal regional perfusion were quantified using laser speckle contrast imaging across placental, umbilical, and multiple fetal vascular beds. In parallel, maternal cardiovascular parameters, including systolic blood pressure and heart weight, and renal parameters, including kidney weight and urinary protein excretion, were assessed, along with fetal and placental biometric measurements and placental angiogenic factors. PE was associated with impaired fetoplacental perfusion and maternal cardiovascular alterations, whereas maternal aerobic exercise was associated with improved fetoplacental microvascular perfusion and attenuation of maternal pathological features. These findings support maternal exercise as a potential non-pharmacological strategy to modulate fetoplacental vascular dysfunction in hypertensive pregnancy.
    Keywords:  Aerobic exercise; Endothelial dysfunction; Fetoplacental microcirculation; Laser speckle contrast imaging; Preeclampsia
    DOI:  https://doi.org/10.1152/japplphysiol.00011.2026
  6. Surg Obes Relat Dis. 2026 May 17. pii: S1550-7289(26)00694-5. [Epub ahead of print]
    The placenta as the missing link in pregnancy after metabolic bariatric surgery.
    Mohamed A Abdelsalam.
      
    DOI:  https://doi.org/10.1016/j.soard.2026.05.013
  7. iScience. 2026 Jun 19. 29(6): 116193
    The Old Lady spider cave skeletons in Ladakh have diverse maternal genetic origin.
    Lomous Kumar, Richa Rajpal, Aparna Dwivedi, Pankaj Kumar, Nagarjuna Pasupuleti, Sachin Kumar, Sonam Spalzin, Stanzen Rabyang, Niraj Rai.
      The archaeological evidence in Ladakh, show early settlement and complex cultural and demographic shifts caused by human migration along the Silk Route corridor, but genetic traces have been entirely absent. To fill this gap, our current study reconstructed complete mitogenomes from ancient individuals found at the Old Lady spider cave site. Our detailed analysis of mitogenomes revealed a highly diverse gene pool that includes maternal lineages associated with East Asia, Central Asia, and South Asia. Bayesian evolutionary analysis, haplotype networks, and divergence times link the C4a1 lineage to East Asia and Siberia, possibly indicating traces of Silk Route migration. Furthermore, these analyses link the H2a1a lineage to recent arrival from Central Asia, while the U7a lineage to a Hazara-like group in Pakistan. These findings point to the maternal genetic imprints of multiple migrations and occupation of the Lady spider cave site in Ladakh by people of diverse maternal lineage.
    Keywords:  Archeology; Evolutionary biology; Paleobiology; Paleogenetics
    DOI:  https://doi.org/10.1016/j.isci.2026.116193
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