bims-placeb 2025-08-10 papers

bims-placeb

Biomed News

on Placental cell biology

Issue of 2025–08–10
thirteen papers selected by
Carlos M Guardia, National Institute of Health

Cultured human stem cells undergoing gastrulation.
Associations of choline intake and metabolite status with fetal growth outcomes and placental macronutrient transport in pregnancies with or without gestational diabetes mellitus.
Establishment of human trophoblast stem cells from term smooth chorion.
From prototype to outbreak: conserved pathogenesis of Oropouche virus in a novel murine pregnancy model highlights its public health implications.
Lipopolysaccharide-induced subclinical infection affects pregnancy and impairs offspring development in an early gestation rat model.
Hypertensive Disorders in Pregnancy.
Open repair versus fetoscopic fetal surgery: Which is the best approach for intrauterine myelomeningocele correction? Systematic review and meta-analysis.
Extracellular vesicles as prospective biological indicators for midgestational placental complications in the mouse.
Potential interactive effect of placental heavy metals and gestational diabetes mellitus on neonatal anthropometric measures: a birth cohort study.
Sex-specific differences in the influence of maternal obesity on the oxidative and inflammatory status in the maternal-placental-fetal unit: new insights into the placental sphingolipid profile.
Hippocampal proteomic signatures of the ketogenic diet in a model of infantile epileptic spasms syndrome.
Trends in fetal autopsy and placental histopathology following stillbirth, United States, 2014-2023.
Study the Effects of Prenatal Exposure to Relaxin-3 on Reflexive Motor Behaviours Development in Mice Offspring.

Cell Res. 2025 Aug 06.

Cultured human stem cells undergoing gastrulation.

Fan Zhang, Fan Guo.

DOI: https://doi.org/10.1038/s41422-025-01151-2
Clin Nutr. 2025 Jul 31. pii: S0261-5614(25)00204-3. [Epub ahead of print]52 179-188

Associations of choline intake and metabolite status with fetal growth outcomes and placental macronutrient transport in pregnancies with or without gestational diabetes mellitus.

Isma'il Kadam, Chauntelle Nebie, Mudar Dalloul, Anjana Saxena, Lawrence Fordjour, Lori Hoepner, Xinyin Jiang.

   BACKGROUND & AIMS: Gestational diabetes mellitus (GDM) is associated with increased risks of fetal overgrowth, possibly due to the increased transport of macronutrients from the placenta to the GDM-exposed fetus. Maternal choline supplementation in obese mice normalizes placental fat and glucose transport and prevents fetal overgrowth. In this study, we aimed to determine the correlation of choline intake and metabolite status with fetal growth outcomes and placental macronutrient metabolism and transport in pregnancies with and without GDM.
METHODS: In this prospective study, we recruited women with (n = 40) and without (n = 36) GDM at 25-33 weeks gestation and assessed their choline intake and blood choline metabolite concentrations. We also collected placenta and cord blood samples from a subset of participants (21 GDM and 26 non-GDM) at delivery to examine placental macronutrient metabolism and transport.
RESULTS: Our results demonstrated that a higher maternal choline intake was associated with lower placental mRNA expression of glucose transporter 3 (GLUT3) (β = -0.002, p = 0.012) in non-GDM pregnancies and leptin (LEP) (β = -0.02, p = 0.034) in GDM pregnancies, respectively. Both maternal blood (β = -77.97, p = 0.03) and placental (β = -0.38, p = 0.049) glycerophosphorylcholine (GPC) concentrations were negatively associated with infant birthweight regardless of GDM status. Maternal GPC concentrations were also negatively associated with placental triglyceride concentrations (β = -0.18, p = 0.017) and cord blood triglyceride (β = -11.1, p = 0.014) and free fatty acid (β = -39.6, p = 0.034) contents, while placental GPC concentrations were negatively associated with fatty acid transporter 1 (FATP1) mRNA expression (β = -1.38E-4, p = 0.036) in all participants. Lipidomics profiling demonstrated that maternal choline intake was negatively associated with concentrations of triglyceride species in the placenta regardless of GDM status.
CONCLUSIONS: In conclusion, maternal choline intakes demonstrated negative associations with placental macronutrient transporters and triglyceride contents. GPC concentrations seem to be a consistent indicator of reduced placental-fetal fat transport and eventually lower birth weight. These observations suggest the potential of using choline to alleviate GDM-related excess in transplacental fat transport and fetal overgrowth.

Keywords:  Birthweight; Choline; Gestational diabetes mellitus; Lipid transport; Placenta

DOI:  https://doi.org/10.1016/j.clnu.2025.07.027
Placenta. 2025 Jul 31. pii: S0143-4004(25)00331-5. [Epub ahead of print]169 114-122

Establishment of human trophoblast stem cells from term smooth chorion.

Takako Hoshiyama, Masanaga Muto, Shoma Matsumoto, Eiichi Okamura, Bat-Erdene Jargalsaikhan, Takashi Murakami, Shunichiro Tsuji, Masatsugu Ema.

   INTRODUCTION: Human trophoblast stem (TS) cells derived from first-trimester placental villi (TSCT) and blastocyst (TSblast) are valuable for studying placental development and pathobiology. However, most placenta-mediated pregnancy complications are diagnosed in the third-trimester, and there are limited reports on TS cells from the third-trimester placental tissues. In this study, we report the successful derivation of TS cells from the term smooth chorion.
METHODS: Smooth chorion isolation was carried out from term placenta, followed by the preparation of single cells through enzymatic dissociation. ITGA6-positive cells were isolated from smooth chorion and cultured in TS medium. The chorion-derived TS (Ch-TS) cells were characterized through flow cytometry, immunocytochemical analysis, DNA methylation analyses via bisulfite sequencing, miRNA analysis using quantitative PCR, and RNA sequencing. To assess their differentiation potential, Ch-TS cells were induced to differentiate into extravillous trophoblast (EVT) cells and syncytiotrophoblast (ST) cells.
RESULTS: Human TS cells were successfully derived from the term smooth chorion. Immunohistochemistry confirmed trophoblast marker expression in Ch-TS cells. Bisulfite sequencing revealed that the ELF5 promoter region was hypomethylated in Ch-TS cells, consistent with trophoblastic DNA methylation status. Ch-TS cells expressed miRNAs from the chromosome 19 miRNA cluster (C19MC). Flow cytometryanalysis revealed that the expression patterns of HLA class I molecules were comparable between Ch-TS and TSCT/blast. Ch-TS cells successfully differentiated into EVT and ST cells. RNA sequencing showed transcriptomic similarities between Ch-TS cells and TSCT/blast cells.
DISCUSSION: Ch-TS cells may serve as a valuable in vitro model for studying trophoblast biology and placenta-mediated pregnancy complications, similar to TSCT/blast cells.

Keywords:  Placenta; Smooth chorion; Term pregnancy; Trophoblast stem cell

DOI:  https://doi.org/10.1016/j.placenta.2025.07.090
bioRxiv. 2025 Aug 02. pii: 2025.08.02.668287. [Epub ahead of print]

From prototype to outbreak: conserved pathogenesis of Oropouche virus in a novel murine pregnancy model highlights its public health implications.

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

Oropouche virus (OROV) is an emerging orthobunyavirus responsible for widespread outbreaks across South and Central America. The recent surge in congenital infections has raised urgent concerns about the threat of OROV to maternal and fetal health. Here, we establish an in vivo model of OROV vertical transmission using the ancestral (prototype) strain BeAn19991 in immunocompetent C57BL/6J mice. We demonstrate that OROV efficiently replicates in maternal tissues, crosses the maternal-fetal interface, and infects both placental and fetal tissues. Parallel infections in human trophoblast-derived cell lines confirm conserved placental tropism across the ancestral strain and a contemporary (outbreak) isolate from the current outbreak. Importantly, we show that vertical transmission is not a recently acquired trait but a long-standing feature of OROV biology. Offspring born to infected dams mount neutralizing antibody responses and exhibit partial protection upon challenge. These findings conclusively confirm OROV as a vertically transmissible arbovirus, highlighting the urgent need to integrate OROV into surveillance, diagnostic, and vaccine preparedness efforts.

DOI: https://doi.org/10.1101/2025.08.02.668287
Placenta. 2025 Jul 29. pii: S0143-4004(25)00318-2. [Epub ahead of print]

Lipopolysaccharide-induced subclinical infection affects pregnancy and impairs offspring development in an early gestation rat model.

J S Beltrame, F Scheffer, V A Cañumil, F L De la Cruz Borthiry, M Cella, M E Bogetti, A M Franchi, M L Ribeiro.

  Subclinical infections cause an imbalance of immune homeostasis that could have severe consequences for pregnancy and progeny development. We investigated if lipopolysaccharide (LPS)-induced subclinical infection affects vascular adaptations during gestation and offspring health. Wistar female rats received intraperitoneal vehicle (saline, control) or low doses of LPS from Escherichia coli (20 μg/kg on day 6 + 50 μg/kg on days 7-9 of gestation). Several parameters were evaluated on day 10 or 15 of pregnancy and the litter. No signs of infection or premature birth were registered after LPS treatment. Maternal survival was not affected by LPS administration. There were no differences in the number of implantation sites or fetuses between groups. However, the blood contained in the uterine and arcuate arteries, and the placentas from LPS-treated mothers exhibited a dark reddish-brown color. Moreover, LPS increased uterine and arcuate arteries' transversal length and decreased the number of vessels in the mesometrial decidua. These vessels showed a larger perimeter. Interestingly, LPS treatment decreased intrauterine fetus growth. No differences were observed in placental efficiency and placental zone areas. An imbalance in the levels of pro-inflammatory cytokines and vascular mediators was detected in the implantation sites and placenta. Furthermore, the offspring showed sex-specific impaired weight gain and neurodevelopment, although maturation milestones were not altered. Our findings show that LPS-induced subclinical infection affects pregnancy and offspring. These alterations are associated with deficiencies in key vascular processes and an imbalance in pro-inflammatory and vascular mediators at the maternal-fetal interface.

Keywords:  Early gestation; Lipopolysaccharide; Offspring; Placenta; Vascular adaptations

DOI:  https://doi.org/10.1016/j.placenta.2025.07.086
Obstet Gynecol Clin North Am. 2025 Sep;pii: S0889-8545(25)00023-3. [Epub ahead of print]52(3): 533-545

Hypertensive Disorders in Pregnancy.

Tabitha Quebedeaux, Jay Davis, Asha J Heard.

  Hypertensive disorders of pregnancy encompass several diagnoses including gestational hypertension, preeclampsia, preeclampsia with severe features, and eclampsia. These disorders occur on a spectrum and can be difficult to predict or prevent. Accurate diagnosis with prompt maternal and fetal assessment and stabilization are a key to timely treatment and optimal disease management.

Keywords:  Aspirin; Chronic hypertension; Eclampsia; Gestational hypertension; Hypertension in pregnancy; Preeclampsia; Preeclampsia with severe features; Superimposed preeclampsia

DOI:  https://doi.org/10.1016/j.ogc.2025.05.006
Childs Nerv Syst. 2025 Aug 08. 41(1): 256

Open repair versus fetoscopic fetal surgery: Which is the best approach for intrauterine myelomeningocele correction? Systematic review and meta-analysis.

Jairo Porfírio de Oliveira Júnior, Bárbara Albuquerque Morais, Matheus Neves Faria Fernandes, Otávio Augusto de Paula Mendes Teixeira, Aloisio Oliveira Lacerda, Milena Vieira Ramos, Rodrigo Akira Watanabe, Paulo Ronaldo Jubé Ribeiro.

   OBJECTIVE: The Management of Myelomeningocele Study in 2011 the prenatal approach has become the gold standard for the correction of myelomeningocele. Since then, advancements in minimally invasive techniques, including fetoscopic repair, have aimed to minimize maternal complications while maintaining fetal benefits.This systematic review and meta-analysis examines the maternal and neonatal outcomes of open versus fetoscopic myelomeningocele repair in utero.
METHODS: We systematically searched PubMed and LILACS databases for studies published between 2011 and 2024, following PRISMA guidelines. Data on maternal and fetal outcomes were extracted and analyzed. A total of 32 studies were included.
RESULTS: Regarding maternal and fetal complications in open and fetoscopic surgery, the rates were respectively: premature rupture of membranes (0.298 95% CI: 0.202-0.393 vs. 0.522 95% CI: 0.254-0.790), oligohydramnios (0.145 95% CI: 0.086-0.203; vs. 0.488 95% CI: 0.162-0.813), premature placental abruption (0.032 95% CI: 0.015-0.048 vs. 0.042 95% CI: 0.0-0.084), birth weight (2261.330 g 95% CI: 2125.819-2369.84; vs. 2251.531 g 95% CI: 1845.674-2657.389), prematurity < 37 weeks (0.789 95% CI: 0.729-0.849 vs. 0.636 95% CI: 0.208-1.064), neonatal sepsis (0.097 95% CI: 0.030-0.163 vs. 0.251 95% CI: 0.046-0.455), surgical time (133.7 min 95% CI: 92.070-175.394 vs. 220.4 min 95% CI: 194.264-246.607), neonatal surgical wound dehiscence (0.043 95% CI: 0.023-0.064 vs. 0.137 95% CI: 0.052-0.222), hydrocephalus (0.422 95% CI: 0.256-0.588 vs. 0.391 95% CI: 0.272-0.510), reversal of brainstem herniation (0.601 95% CI: 0.385-0.816 vs. 0.581 95% CI: 0.356-0.806), maintenance or improvement in motor function (0.809 95% CI: 0.692- 0.927 vs. 0.856 95% CI: 0.734-0.978). Only neonatal sepsis in the fetoscopic surgery group was not statistically significant (p < 0.05).
CONCLUSIONS: The open approach, traditionally associated with better fetal outcomes, showed better outcomes for maternal complications compared to fetoscopic surgery.

Keywords:  Fetal neurosurgery; Fetoscopic; Meta analysis; Myelomeningocele; Open repair; Spina bifida

DOI:  https://doi.org/10.1007/s00381-025-06915-0
Front Cell Dev Biol. 2025 ;13 1636335

Extracellular vesicles as prospective biological indicators for midgestational placental complications in the mouse.

Elaine Lee, Parinaz Kazemi, Shiva Shafiei, Sarah Yull, Mansuba Rana, Nadim Tawil, Laura Montermini, Janusz Rak, Daniel Dufort.

   Background: Placental dysfunction is often associated with reproductive complications such as preeclampsia, intrauterine growth restriction (IUGR), and preterm birth. Currently, the early diagnosis and intervention of these pathologies remain challenging due to the invasive nature of placental tissue sampling. Liquid biopsies of extracellular vesicles (EVs) released from the placenta have emerged as a prospective minimally invasive diagnostic strategy that could provide insight into the maternal-fetal interface because of the active role EVs play in mediating placental development and function. However, the lack of information on EVs directly from placenta at disease onset has questioned the representativeness of placental EVs as pathological indicators. To address these concerns, this study assessed the accuracy with which tissue-derived D10.5 placental EVs could identify phenotypes exhibited by a reproductively challenged Nodal conditional knockout mouse model at mid-gestation.
Method: Implantation sites from female mice with a uterine-specific knockdown of the Nodal gene were examined from D8.5 to D14.5 utilizing histological analysis, Western blotting, and RT-qPCR to characterize their mid-gestational phenotypes. Placental EVs were then isolated from D10.5 placenta using enzymatic digestion, differential centrifugation, filtration, and size-exclusion chromatography. The final EV fractions were concentrated and validated with size analysis, canonical protein markers, and morphology assessment. Differential expression analysis across the EV samples was performed using proteomics and miRNA-Seq. Functional enrichment analysis of dysregulated EV factors was then completed using several gene ontology databases along with a literature review to determine whether placental EVs could indicate the reproductive abnormalities presented by the mutant mice.
Results: Uterine-specific deletion of Nodal resulted in IUGR and fetal loss in mutant dams. Decidualization and placentation defects were observed, including thinner decidual and placental tissues, impaired angiogenesis, and an altered junctional zone within the maternal-fetal interface. Bioinformatics analysis of EV cargo identified 31 differentially expressed proteins and 10 miRNAs specifically linked to placental development, oxidative stress, angiogenesis, and immunomodulation. Notably, 15 of these proteins and six of these miRNAs have been previously associated with pregnancy complications, further supporting the prospects of placental EVs as biomarkers for various placental diseases.
Conclusion: These findings suggest that placental EVs can reflect compromised placental function and could serve as pathological indicators for the early detection of pregnancy complications. Their potential diagnostic utility could improve maternal and neonatal health outcomes by enabling earlier intervention and monitoring of high-risk pregnancies.

Keywords:  EVs; Nodal; exosomes; miRNAs; placenta; pregnancy; proteomics

DOI:  https://doi.org/10.3389/fcell.2025.1636335
Environ Pollut. 2025 Jul 31. pii: S0269-7491(25)01303-X. [Epub ahead of print]384 126930

Potential interactive effect of placental heavy metals and gestational diabetes mellitus on neonatal anthropometric measures: a birth cohort study.

Shidie Chen, Jixing Zhou, Mengjie Zhu, Juan Tong, Chunmei Liang, Xiaoyan Wu, Guopeng Gao, Shuangqin Yan, Fangbiao Tao, Kun Huang.

  Studies demonstrate that prenatal exposure to heavy metals can impair fetal growth and development. Meanwhile, gestational diabetes mellitus (GDM), a frequent pregnancy complication, may also influence fetal development. Given the potential coexistence of these two risk factors, further investigation is needed to elucidate their combined effects on fetal development. Therefore, the current study aims to examine the relationship between mixed metal exposure and neonatal anthropometric measures under different maternal GDM status. Based on the Ma'anshan Birth Cohort (MABC), our study included 2397 mother-child pairs. Seven metals in the placenta were tested: arsenic(As), cobalt(Co), chromium(Cr), lead(Pb), cadmium(Cd), mercury(Hg) and zinc(Zn). Regression models, weighting indices, and mixed exposure models were used to analyze the association of metals and neonatal anthropometric measures, and relevant sensitivity analyses were conducted. In the GDM group, placental Zn was associated with a decreased risk of Small for Gestational Age (SGA) (OR = 0.20, 95 %CI: 0.05-0.83), while Hg was associated with an increased risks of SGA (OR = 3.18, 95 %CI: 1.38-7.35) and Large for Gestational Age (LGA) (OR = 2.11, 95 %CI: 1.09-4.12). We found a U-shaped relationship between mixed metal exposure and birth weight in the non-GDM group. While in the GDM group, an increase in the concentration of mixed metal exposure was associated with an increase in birth weight. In the non-GDM group, a decreased risk of low birth weight(LBW) was observed in Co (OR = 0.13, 95 %CI: 0.04-0.43), while an increased risk was observed in Hg (OR = 2.06, 95 %CI: 1.11-3.83) and Cr (OR = 1.87, 95 %CI: 1.04-3.35) exposure, with no significant associations in GDM. High mixed concentrations were found to be related to increased birth length in GDM group, but related with decreased birth length in non-GDM group. The association between placental heavy metals and neonatal anthropometric measures differed between GDM and non-GDM group. These observations warrant further experimental studies to elucidate the underlying mechanisms.

Keywords:  Gestational diabetes mellitus; Neonatal anthropometric measures; Newborn; Physical development; Placental metals

DOI:  https://doi.org/10.1016/j.envpol.2025.126930
Mol Cell Endocrinol. 2025 Aug 06. pii: S0303-7207(25)00191-1. [Epub ahead of print] 112640

Sex-specific differences in the influence of maternal obesity on the oxidative and inflammatory status in the maternal-placental-fetal unit: new insights into the placental sphingolipid profile.

Marta Hita Hernández, Esther Dos Santos, Yoann Rodriguez, Véronique Ferchaud-Roucher, Delphine Rousseau-Ralliard, Anne Frambourg, Paul Berveiller, François Vialard, Anne Couturier-Tarrade, Marie-Noëlle Dieudonne.

  Although maternal obesity influences placental and fetal development, the underlying molecular mechanisms have yet to be determined. Oxidative and inflammatory status at the fetal-placental unit appear to be involved in the early fetal metabolic programming. The objective of the present study is to reveal a potential role of sphingolipids in stablishing an oxidative and inflammatory status in the maternal-placental-fetal unit, as function of fetal sex. Term placenta and maternal and fetal plasma were collected from lean (BMI 18-25 kg/m2) and obese women (BMI 30-40 kg/m2) without gestational diabetes aged from 20 to 40 having undergone a cesarean section. Firstly, key markers of oxidative stress and inflammation were studied with immunoblotting and biochemical assays. Secondly, the maternal-placental-fetal unit's sphingolipid profile was determined by mass spectrometry. Lastly, the placental samples' transcriptome was analyzed by RNA sequencing. Obese mothers showed lower plasma levels of ceramide Cer 20:0 (p=0.02). Surprisingly, placental ceramide content was not influenced by maternal obesity. Nevertheless, male placentas from obese women showed a higher sphingomyelin content and hypo-inflammation as showed by RNAseq. Both males and female placentas from obese women showed higher levels of oxidative stress as showed by the oxidative stress markers (protein carbonylation and lipid peroxidation). However, RNAseq revealed an upregulation of oxidative stress mechanisms only in female placentas. Whatever the newborn's sex, maternal obesity was associated with higher fetal plasma oxidative stress. In conclusion, our results revealed sex-specific features in the placental transcriptome, highlighted placental metabolic adaptations, and provided insights into the underlying molecular mechanisms of fetal programming.

Keywords:  Maternal obesity; fetal sex; maternal-placental-fetal unit; placental sphingolipids

DOI:  https://doi.org/10.1016/j.mce.2025.112640
Biochim Biophys Acta Mol Basis Dis. 2025 Aug 05. pii: S0925-4439(25)00359-X. [Epub ahead of print] 168011

Hippocampal proteomic signatures of the ketogenic diet in a model of infantile epileptic spasms syndrome.

Jaclyn C Campbell, Chunlong Mu, Tina R Ram, Daniel Young, Antoine Dufour, Morris H Scantlebury, Jane Shearer.

  Infantile epileptic spasms syndrome (IESS) is a rare, early-onset pediatric epilepsy with severe neurological consequences. In refractory cases, the ketogenic diet (KD) is used as a metabolic therapy. To understand the antiepileptic mechanisms of the diet, this study examined the proteomic profiles in the hippocampus after KD treatment. Utilizing a rodent model of IESS in combination with quantitative proteomics, this study showed that the KD upregulated proteins involved in synaptogenesis, mitochondrial function, and neuroinflammation. Preliminary investigation reveals the KD induces alterations in hippocampal protein expression that mitigate neurodevelopmental consequences, providing candidate targets for future IESS investigation.

Keywords:  Epilepsy; Hippocampus; Infantile epileptic spasms syndrome; Ketogenic diet; Proteomics

DOI:  https://doi.org/10.1016/j.bbadis.2025.168011
J Perinatol. 2025 Aug 07.

Trends in fetal autopsy and placental histopathology following stillbirth, United States, 2014-2023.

Sabrina Montgomery, Katherine Bianco, Elizabeth B Sherwin, Hayley E Miller, Ruth B Lathi, Stephanie A Leonard.

DOI: https://doi.org/10.1038/s41372-025-02381-3
Int J Dev Neurosci. 2025 Aug;85(5): e70033

Study the Effects of Prenatal Exposure to Relaxin-3 on Reflexive Motor Behaviours Development in Mice Offspring.

Zahra Shaddel, Morteza Zendehdel, Hamed Zarei, Shahin Hassanpour.

  Relaxin-3 is a member of a structurally related peptide superfamily that includes relaxin and insulin-like peptide hormones, which play a role in regulating stress, memory, nutrition, pregnancy and childbirth, mental illnesses, including anxiety, depression and schizophrenia, cardiovascular protective effects, and regulating social behaviour and nutritional behaviour of children with autism. However, there is no information about the effect of relaxin-3 during pregnancy on the development of behavioural and motor reflexes in mice offspring. This study aims to determine the effects of prenatal exposure to relaxin-3 on reflexive motor behaviours in mice offspring. Twelve pregnant female NMRI mice (8-10 weeks old) were randomly and equally allocated into four groups. In the control group, mice received water, while in groups 2-4, female mice were i.p. administered relaxin-3 (12.5, 25 and 50 μg/kg) at 5, 8, 11, 14 and 17 days of gestation (GD). Following delivery, 10 pups from each pregnant mouse were selected, and reflexive motor behaviours including ambulation, hind-limb foot angle, surface righting, grip strength, front- and hind-limb suspension, and negative geotaxis were determined. Based on the findings, maternal exposure to relaxin-3 promoted an increase in ambulation scores and hind-limb suspension in offsprings (p < 0.05). Also, maternal exposure to relaxin-3 (25 and 50 μg/kg) promoted an increase in grip strength and front limb suspension scores in newborns (p < 0.05). Maternal exposure to relaxin-3 decreased surface righting (p < 0.05). Prenatal exposure to relaxin-3 (25 and 50 μg/kg) decreased hind-limb foot angle and negative geotaxis in pups (p < 0.05). These results suggested that relaxin-3 exposure during pregnancy had a positive effect on all tested reflexive motor behaviours in mice offspring.

Keywords:  mice offspring; prenatal; reflexive motor behaviours; relaxin‐3

DOI:  https://doi.org/10.1002/jdn.70033