bims-placeb Biomed News
on Placental cell biology
Issue of 2025–12–07
twelve papers selected by
Carlos M Guardia, National Institute of Environmental Health Sciences



  1. J Physiol Pharmacol. 2025 Aug;76(4): 459-471
      Vaspin, a visceral-adipose-tissue-derived serine protease inhibitor, is involved in the development of obesity, insulin resistance, energy metabolism, and reproduction. Its expression and regulation were studied in the human and rat placenta; however, the role of this adipokine in placental endocrine function has never been studied. The present study aimed to investigate the in vitro effects of vaspin on the endocrine function of the human placental syncytiotrophoblasts BeWo cell line and villous explants collected during the third trimester of pregnancy. BeWo cells (n=4) or villous explants (n=3) were cultured with vaspin at doses of 0.1, 1, and 10 ng/ml for 24, 48, and 72 h. The levels of progesterone (P4), estradiol (E2), human chorionic gonadotropin (hCG), and human placental lactogen (hPL) were determined in the culture medium via enzyme-linked immunosorbent assay (ELISA). In addition, the mRNA and protein expression of 3β-hydroxysteroid dehydrogenase (HSD3B1/3βHSD), aromatase (CYP19A1/CYP19), CGB3/hCG, and CSH1/hPL were determined via real-time PCR and Western blotting, respectively. We analyzed the role of pharmacological inhibitors of extracellular signal-regulated kinase (ERK1/2) and protein kinase A (PKA) in the vaspin action on hormone secretion. We observed that vaspin has a modulatory effect on the secretion and expression of placental hormones in BeWo cells and placentas from physiological pregnancies. However, in most cases, the effect was inhibitory on the parameters examined. Moreover, we noted that PKA participates in reducing E2 secretion, while ERK1/2 is involved in hCG level. These findings indicate that vaspin is a new regulator of human placental endocrine function.
    Keywords:  endocrinology; estradiol; extracellular signal-regulated kinase; human chorionic gonadotropin; human placental lactogen; progesterone; protein kinase A; trophoblast; vaspin
    DOI:  https://doi.org/10.26402/jpp.2025.4.09
  2. Biol Open. 2025 Dec 04. pii: bio.062296. [Epub ahead of print]
      Down syndrome (DS) is caused by trisomy for human chromosome 21 (Hsa21) and is associated with atypical neurodevelopment that begins prenatally. The developing human fetus receives nutritional support and gas exchange from the placenta, and normal placental function is essential for proper development. Placentas that sustain fetuses with trisomy 21 contain trisomic cells, but little is known about which Hsa21 genes are overexpressed in the placenta or their downstream molecular, cellular, and functional effects. Although access to human placentas is limited, mouse models of DS provide excellent in vivo systems for investigating the prenatal effects of trisomy. This study examined the placental transcriptome in four mouse models of DS: Dp(16)1/Yey, Ts65Dn, Ts66Yah, and Ts1Cje. Placental gene and protein expression analyses showed that trisomy increased the expression of App, Sod1, and Ifnar1 in Dp(16)1/Yey, Ts65Dn, and Ts66Yah, APP and SOD1 in Dp(16)1/Yey and Ts66Yah, and IFNAR1 in Ts66Yah. Despite modest overlap of trisomy-associated gene dysregulation among these four models, altered extracellular matrix pathways in all four models and upregulation of immune system pathways in Dp(16)1/Yey and Ts66Yah were identified. Altered redox homeostasis was observed for all four models, with Ts1Cje showing distinct changes in SOD activity and antioxidant capacity in comparison to the other three models. Immunofluorescence staining revealed region-specific upregulation of APP, SOD1, and IFNAR1 in Ts66Yah trisomic placentas. This work provides a foundation for understanding the effects of trisomy for Hsa21 orthologs on the mouse placenta and on prenatal development.
    Keywords:  Down syndrome; Mouse models; Transcriptomics; Trisomy 21
    DOI:  https://doi.org/10.1242/bio.062296
  3. Placenta. 2025 Dec 03. pii: S0143-4004(25)00762-3. [Epub ahead of print]174 53-62
       INTRODUCTION: The pregnancy disorder preeclampsia (PE) is characterized by maternal hypertension and reduced spiral artery (SpA) remodeling which is aggravated by increased levels of anti-angiogenic soluble fms-related tyrosine kinase 1 (sFLT1). One process contributing to physiological SpA remodeling in early pregnancy is the expression of lymphatic receptors on endothelial cells of SpAs, which is called lymphatic mimicry. Adverse lymphatic mimicry of SpAs is theorized to play a role in the pathophysiology of PE, but was not analyzed under preeclamptic conditions.
    METHODS: Using the transgenic PE/FGR mouse model with ubiquitous overexpression of human sFLT1 (hsFLT1), we focused on lymphatic marker expression in early pregnancy at 12.5 dpc and 14.5 dpc and evaluated the reduction of SpA remodeling as well as mRNA expression of lymphatic markers like Lyve1, Pdpn, or Prox1 in the mesometrial triangle (MT) of murine placentas. Additionally, uterine NK cell distribution was analyzed via electron microscopy and immunohistochemistry in placentas of PE animals.
    RESULTS: We could prove significantly reduced levels of Pdpn and Nrp1 mRNA in MT of PE placentas. Additionally, the mRNA expression of chemokines like Ccl21 were reduced at from 12.5 dpc until 14.5 dpc which could inhibit infiltration of uterine NK cell populations in these compartments in later pregnancy.
    DISCUSSION: With this study we could show that increased levels of human sFLT1 interfere with early spiral artery (SpA) remodeling processes and could inhibit lymphatic mimicry of SpA. Immune cell infiltration until 14.5 dpc could be decreased by downregulation of the chemotactic chemokine Ccl21.
    Keywords:  Lymphangiogenesis; Lymphatic mimicry; Placenta; Preeclampsia; Spiral artery remodeling; sFLT1
    DOI:  https://doi.org/10.1016/j.placenta.2025.12.002
  4. Hum Mol Genet. 2025 Nov 30. pii: ddaf143. [Epub ahead of print]
      The occurrence of preterm premature rupture of membranes (PPROM) significantly impacts maternal and fetal health due to its association with the cellular composition and genetic changes of the fetal membrane. However, the specific cell type responsible for triggering PPROM and the underlying mechanisms are still largely unexplored. We employed single-cell RNA sequencing (scRNA-seq) analysis on fetal membrane along with adjacent placental tissues about two centimeters from the umbilical cord obtained from women who delivered full-term in labor (FTIL), preterm premature without rupture of membrane (PPWROM), as well as PPROM,immunofluorescence were used to verify the findings. Our result s highlighted notable differences in cell type composition and interactions among these three groups. Of particular significance, we have identified a previously unrecognized subtype of trophoblast cells known as FABP7+Tb, a transitional state cell between cytotrophoblasts (CTB) and extravillous trophoblasts (EVT) cells, which appears to have some impact on PPWROM. Additionally, up-regulated expression of MMP11 in EVT-1 may serve as a promising biomarker for PPROM diagnosis. Furthermore, our study unveiled distinct interaction patterns among different trophoblast subtypes under varying pathological conditions, as well as significant variations in the interactions of trophoblast cells with other cell types, especially the pathways that are orchestrated by cell-cell cross-talk. Our study offers a comprehensive cell type and interaction map for the human fetal membrane along with adjacent placental tissues about two centimeters from the umbilical cord, providing insights into the molecular mechanisms that drive PPROM and uncovering potential targets for the early prediction of this condition.
    Keywords:  fetal membrane; placenta; preterm rupture of membranes; single-cell RNA sequencing; trophoblast cells
    DOI:  https://doi.org/10.1093/hmg/ddaf143
  5. Front Pharmacol. 2025 ;16 1673124
       Introduction: Generally, the pregnant women with schizophrenia have higher consumption of medicinal drugs. During pregnancy, placental ABC transporters regulate drug disposition and are involved in fetal and placental development. This study examined the expression and function of placental P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) transporters in vivo and evaluated the epigenetic impact of schizophrenia on the placenta in a rat model.
    Methods: The expression of placental P-gp and BCRP was measured by RT-PCR and Western blot techniques in schizophrenia-like Wisket and control Wistar rats on gestation days 15, 18, 20, 21, and 22, while the histone acetyltransferase activity and global methylation state of the placenta were detected by colorimetric kits. Fexofenadine was administered per os (10 mg/kg) to pregnant rats and plasma concentrations of fexofenadine were determined with HPLC analysis on the 21 and 22 days of gestation.
    Results: Reduced placental P-gp expression was identified in late pregnancy, while the placental BCRP expression upregulation was observed before term in schizophrenia. Significantly lower fetal fexofenadine plasma concentration was measured on the 21st and 22nd days of pregnancy compared to the mother; in contrast, the fexofenadine concentration was similar in the schizophrenia-like mother and fetus. Decreased placental histone acetyltransferase activity and DNA hypermethylation were revealed before term in schizophrenia-like rats.
    Conclusion: Based on our results, we can conclude that the expression and function of the placental efflux proteins we examined are altered in schizophrenia, and possibly as a result, altered substrate concentrations were measured in the fetuses. We hypothesize that the altered protein expression may also be a result of the disease-induced epigenetic pattern changes. This study presents novel disease-associated placental ABC transporter alterations, which highlights the dangers of using transporter substrates, especially P-gp, during pregnancy.
    Keywords:  P-glycoprotein; breast cancer resistance protein; epigenetic; fexofenadine; placenta; rat; schizophrenia
    DOI:  https://doi.org/10.3389/fphar.2025.1673124
  6. Gene. 2025 Dec 03. pii: S0378-1119(25)00722-X. [Epub ahead of print] 149932
      Syncytin-2 is an endogenous retroviral envelope protein constitutively expressed in human placental trophoblasts. As a membrane glycoprotein, Syncytin-2 together with Syncytin-1 mediates the fusion of mononucleated cytotrophoblasts to form multinucleated syncytiotrophoblasts. Syncytiotrophoblasts constitute the fetal-maternal interface important for fetal-maternal exchange, barrier and endocrine functions of the placenta. Besides the fusogenic function, Syncytin-2 also possesses an immunosuppressive activity. In this study, the results of quantitative PCR indicated that Syncytin-2 expression was downregulated in third-trimester preeclamptic placentas, which is consistent with the result of previous studies. Importantly, the results of Combined Bisulfite Restriction Assay (COBRA) suggested hypermethylation of the downstream CpG-rich region, but not the promoter/exon1/intron1 and exon2 CpG- rich regions of SYN-2 gene in third-trimester preeclamptic placentas. Subsequent bisulfite conversion and PCR amplification, cloning and sequencing of the downstream CpG- rich region confirmed hypermethylation of the 4 CpGs in this region in preeclamptic placentas. Moreover, treatment of human choriocarcinoma BeWo cells with DNMT inhibitor ADC (5-aza-deoxycytidine) resulted in a dose-responsive demethylation of the downstream CpG-rich region and an increased SYN-2 mRNA level. Thus, the hypermethylation of the downstream CpG-rich region closely correlated with the downregulation of Syncytin-2 expression in preeclamptic placentas. These new findings underscore the significance of epigenetic alterations in preeclamptic placentas, and facilitate a better understanding on the pathological mechanism of preeclampsia.
    Keywords:  CpG; DNA hypermethylation; Downregulation; Placenta; Preeclampsia; Syncytin-2
    DOI:  https://doi.org/10.1016/j.gene.2025.149932
  7. PLoS One. 2025 ;20(12): e0337568
       BACKGROUND: Polystyrene nanoparticles (PS-NPs) are recognized as environmental pollutants with potential reproductive toxicity. This study delves into the impacts of PS-NPs exposure on trophoblast cells, specifically examining mitochondrial dysfunction, cell invasion and migration.
    METHODS: Trophoblast cells were exposed to PS-NPs to evaluate the effects on cell proliferation, apoptosis, mitochondrial function (including mitochondrial membrane potential, intracellular ROS levels, and gene expression), autophagy, inflammatory responses and cell motility. Co-immunoprecipitation and Western blotting analyses were employed to assess the expressions and interactions of MDM2 and ROCK1 under PS-NPs exposure conditions.
    RESULTS: We observed that PS-NPs exposure impaired trophoblast cell proliferation, promoted apoptosis, and disrupted mitochondrial function, evident by ROS elevation, mitochondrial membrane potential reduction, and altered gene expression. Increased autophagy activity and inflammatory cytokine release indicated cellular stress. Moreover, PS-NPs impeded cell migration and invasion, with exacerbated effects upon MDM2 knockdown and ROCK1 inhibition.
    CONCLUSION: The study elucidates the intricate connections among mitochondrial dysfunction, autophagy, inflammation, and cell motility in response to PS-NPs, suggesting that targeting the MDM2-ROCK1 pathway could offer a promising approach to alleviate PS-NP-induced toxicity in trophoblast cells and support placental health.
    DOI:  https://doi.org/10.1371/journal.pone.0337568
  8. Physiol Rep. 2025 Dec;13(23): e70684
      Archaeological and anthropological evidence suggests that human ancestors' diets were rich in fiber, potassium, and complex carbohydrates, while low in sodium, refined sugars, and energy density. Over time, agroindustrialization led to diets poorer in fiber and micronutrients but higher in sodium, simple sugars, and calorie-dense foods. This shift contributed to the rise of noncommunicable diseases (NCDs) such as obesity, type 2 diabetes, and cardiovascular diseases, which now account for 70% of global premature deaths. Maternal nutrition affects fetal development and long-term health. High sucrose or fructose intake during pregnancy can alter placental function, impacting fetal growth and metabolism. Placentae from male and female fetuses may respond differently to maternal diet. However, the effects of excessive maternal fructose intake on the placenta and offspring remain underexplored. In this study, rat dams consuming fructose-sweetened beverages ate less food but drank more, significantly impacting placental volume and vascular structure. Long-term effects on offspring were sex-specific: females showed greater water retention and liver fat accumulation. High maternal fructose intake altered placental anatomy and had sex-specific effects on kidney and liver function in adult offspring, even without further fructose exposure. These findings highlight the importance of maternal diet in preventing future metabolic diseases.
    Keywords:  beverage; fructose; kidney; liver; rat
    DOI:  https://doi.org/10.14814/phy2.70684
  9. Cell. 2025 Dec 03. pii: S0092-8674(25)01255-3. [Epub ahead of print]
      While non-mammalian embryos often rely on spatial pre-patterning, mammalian development has long been thought to begin with equivalent blastomeres. However, emerging evidence challenges this. Here, using multiplexed and label-free single-cell proteomics, we identify over 300 asymmetrically abundant proteins-many involved in protein degradation and transport-dividing mouse 2-cell-stage blastomeres into two distinct clusters, which we term alpha and beta. These proteomic asymmetries are detectable as early as the zygote stage, intensify by the 4-cell stage, and correlate with the sperm entry site, implicating fertilization as a symmetry-breaking event. Splitting 2-cell-stage embryos into halves reveals that beta blastomeres possess greater developmental potential than alpha blastomeres. Similar clustering and protein enrichment patterns found in human 2-cell embryos suggest this early asymmetry might be conserved. These findings uncover a previously unrecognized proteomic pre-patterning triggered by fertilization in mammalian embryos, with important implications for understanding totipotency and early lineage bias.
    Keywords:  2-cell blastomere asymmetries; developmental biology; embryonic patterning; epiblast; human development; lineage specification; mammalian embryonic development; pre-implantation development; single-cell proteomics by mass spectrometry; totipotency
    DOI:  https://doi.org/10.1016/j.cell.2025.11.006
  10. J Anim Sci. 2025 Jan 04. pii: skaf374. [Epub ahead of print]103
      Low birth weight (LBW) has been an important problem in animal husbandry, contributing to high mortality and morbidity rates in the neonatal period. To explore the mechanism regulating placental function and fetal development, paired normal birth weight (NBW, 1.54 ± 0.08 kg) and LBW (0.95 ± 0.16 kg) piglets (n = 10) were selected from ten gilts. Serum biochemistry indexes and placental transport capacity were measured. Placental and serum samples of sows or piglets were collected, and the characteristics of sows and piglets were recorded. Furthermore, this study utilized porcine trophoblast cells (pTrs) as a model to investigate the effects of cortisol (0, 0.01, 0.1, and  pg/mL) on cell viability, migration, glucose transport, gene and protein expression. Additionally, rapamycin (20 nmol/L) was used to inhibit the activity of mammalian target of rapamycin complex 1 (mTORC1). All experiments were independently repeated at least three times. Data were analyzed using SAS (version 9.4). An unpaired t-test was applied to compare values between the LBW and NBW piglets. Student's t-tests were used for single comparisons in cell experiments. Significance was declared at P < 0.05. Results showed that LBW piglets had reduced levels of glucose, cortisol, Phe, Val, Ile, Leu, Met, and homocysteine compared to NBW piglets (P < 0.05). Moreover, the placental expression of Glut1 and Slc43a2 were significantly downregulated (P < 0.05), and mTORC1 signaling pathway was inhibited (P < 0.05) in LBW piglets compared with NBW piglets. Furthermore, birth weight of piglets was positively correlated with cortisol levels (P < 0.01, r = 0.58). Further results found that cortisol activated the protein expression of p-S6K1 (P < 0.05) and upregulated the protein expression of GLUT3, LAT2, and SLC6A19 (P < 0.05), and increased the glucose transport rate and number of cell migrations (P < 0.05). However, rapamycin supplementation downregulated the protein expression of p-S6K1 (P < 0.05) and reduced the number of cell migration (P < 0.05) in the cortisol group. Overall, these results suggest that cortisol improves the placental glucose and amino acid transport via the mTORC1 signaling pathway.
    Keywords:  amino acids; cortisol; glucose; low birth weight; piglets; placental transport
    DOI:  https://doi.org/10.1093/jas/skaf374
  11. Hum Reprod. 2025 Dec 03. pii: deaf235. [Epub ahead of print]
       STUDY QUESTION: Can comprehensive cytogenetic follow-up of the placenta post-partum uncover possible explanations for discrepancies between non-invasive prenatal testing (NIPT) showing structural chromosomal aberrations and foetal follow-up showing normal results or other chromosomal aberrations?
    SUMMARY ANSWER: In 18/31 (58%) cases of structural chromosomal aberrations detected with NIPT, where foetal and maternal follow-up was normal or the foetus had another chromosomal aberration, genome-wide examination of term placental chorionic villi confirmed the discrepancy and in 7/18 (39%) confirmed cases complex foeto-placental mosaicism was found.
    WHAT IS KNOWN ALREADY: Complex chromosomal rearrangements are often seen in single-cell studies of preimplantation embryos, but it is unknown if these persist into the mature placenta. Confined placental mosaicism explains most discordant NIPTs involving a trisomy, but little is known about structural chromosome aberrations.
    STUDY DESIGN, SIZE, DURATION: We performed a retrospective diagnostic test study of cytogenetic follow-up data from post-partum placentas. We included data from pregnancies where (i) NIPT showed a structural aberration, (ii) follow-up of foetus (amniotic fluid and/or cord blood) and mother (genomic DNA and/or cfDNA after birth) was normal or the foetus showed another chromosomal aberration, (iii) follow-up was performed in the Erasmus MC, (iv) more than one sample from the post-partum placenta was analysed, and (v) samples were of good quality (not in formaldehyde, sufficient material).In the period from January 2014 to March 2022, 115 231 NIPTs were performed in the Erasmus MC; 217 of these showed structural chromosomal aberrations and 123 were followed up in the Erasmus MC (inclusion criteria 3). After exclusion of the foetal (same aberration as with NIPT) and maternal structural chromosome aberrations, 48 placentas were requested to elucidate the discrepancies seen between NIPT (abnormal) and foetal karyotype (normal or differently abnormal; inclusion criteria 1-2). Of these, 31 met criteria 4 and 5 and were included in this study.
    PARTICIPANTS/MATERIALS, SETTING, METHODS: In a diagnostic setting, we performed a cytogenetic analysis of postpartum placentas in order to confirm confined placental mosaicism in 31 cases in which NIPT showed a structural chromosome aberration. Two to four chorionic villus biopsies were taken per placenta, and separated enzymatically into cytotrophoblast (CTB) and mesenchymal core (MC) and analysed using SNP arrays. In our analysis, cases were assessed for copy number variants ≥0.5 Mb and regions of homozygosity ≥3 Mb.
    MAIN RESULTS AND THE ROLE OF CHANCE: In 18/31 cases (58%), we could confirm the structural chromosome aberration detected with NIPT in one or more placental biopsies. In 13/31 cases (42%), the structural chromosomal aberration detected with NIPT was not confirmed, but in one case an apparently unrelated aberration was found in the CTB of two biopsies. In 11/18 confirmed cases, the same aberration as detected with NIPT, was confirmed in the placenta. All these cases concerned chromosomally normal foetuses with a chromosome aberration confined to the placenta. In one case, an extra, apparently unrelated, aberration was found in one placental biopsy. In 7/18 confirmed cases, the aberration detected with NIPT was confirmed in the placenta and showed to be involved in complex mosaicism involving different abnormal cell lines. In four of these seven cases, the foetus was affected with a pathogenic chromosome aberration that was different from the NIPT aberration. In three cases, a related but benign chromosome aberration was present in the foetus.
    LIMITATIONS, REASONS FOR CAUTION: As conventional karyotyping, FISH or whole genome sequencing were not performed, we can only hypothesize on the mechanisms behind the origin of the complex foeto-placental mosaicism we see in seven cases, although there is more strong evidence in the literature as well.
    WIDER IMPLICATIONS OF THE FINDINGS: Our results have several implications. First, a genome-wide rather than a targeted approach in foetal follow-up examinations after NIPT showing a structural chromosomal aberration is warranted, as other aberrations may be overlooked in the foetus. Second, counselling of pregnant couples after NIPT showing a structural chromosomal aberration should focus not only on the specific aberration detected by NIPT but also on the possibility that the foetus may harbour another, possibly related, structural aberration. Additionally, a structural chromosomal aberration of apparently uncertain significance may unmask truly pathogenic aberrations in the foetus itself, so all potential foetal cases of structural chromosome aberrations should be followed up. Third, we show how comprehensive examinations of the placenta, specifically the separation of CTB and MC, provides crucial insights into the embryonic origins and mechanisms behind structural chromosomal aberrations. Lastly, our results show that complex chromosomal rearrangements as often seen in single-cell studies of pre-implantation embryos, are not artefacts but a biological phenomenon that can actually persist into the mature placenta and foetus.
    STUDY FUNDING/COMPETING INTEREST(S): Simon H. Thomsen was funded by a private research donation and the Department of Clinical Medicine, Aarhus University. All authors declare no conflict of interest.
    TRIAL REGISTRATION NUMBER: N/A.
    Keywords:  NIPT; confined placental mosaicism; placenta; prenatal diagnosis; structural chromosomal aberrations
    DOI:  https://doi.org/10.1093/humrep/deaf235
  12. Nature. 2025 Dec 03.
      Stem cell-derived embryo models could greatly facilitate our understanding of embryonic development. Although human and monkey embryo models have reached early gastrulation stage1-7, the development of robust models beyond this time remains to be accomplished8. Here, using an optimized 3D suspension culture system, we have successfully advanced the in vitro culture of a stem cell-derived monkey blastoid to day 25. Morphological and histological analyses showed that these monkey embryoids underwent gastrulation and largely recapitulated key developmental events of the late gastrulation stage observed in vivo, with the appearance of a neural plate, haematopoietic system, allantois, primitive gut, primordial germ cells, yolk sac structures and progenitors of other organs, excluding trophoblast derivatives. Single-cell transcriptomic analyses revealed that the lineage composition and differentiation trajectories of cells in these monkey embryoids were similar to those found in natural embryos during gastrulation. Thus, this primate stem cell-derived embryo model provides a valuable platform for dissecting the mechanisms of primate embryonic development from blastocyst to late gastrulation stage.
    DOI:  https://doi.org/10.1038/s41586-025-09831-0