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Home / Equine Research Bank / Sci Rep / Decoding the amniotic membrane transcriptome during equine a...
Scientific reports2025; 15(1); 30714; doi: 10.1038/s41598-025-16671-5

Decoding the amniotic membrane transcriptome during equine ascending placentitis.

Abstract: Despite its critical role in protecting the fetus, the amniotic membrane remains poorly understood in the context of disease response. The equine amniotic membrane is an important physical barrier to the amniotic compartment, and there is evidence that it may contribute to surfactant synthesis. Surfactants are essential for normal fetal lung development, and disruptions in its availability may be linked to future neonatal complications. Therefore, understanding the molecular changes that occur in fetal-maternal tissues during placentitis would clarify how this condition leads to abortion, preterm delivery, and stillbirth, and identify new strategies to manage the adverse outcomes. Thus, we used RNA sequencing, bioinformatic methods, and immunohistochemistry to characterize the equine amniotic membrane gene expression during experimentally induced ascending placentitis (placentitis group, n = 6) compared to gestationally matched control groups (control group, n = 6) at 288 days of gestation. We identified 288 differentially expressed genes (DEG) in the placentitis group compared to the control group. Placentitis was associated with the upregulation of toll-like receptors (TLR4), prostaglandin synthesis (PTGS2 and PTGES), apoptosis (MMP9 and CASP3), and hypoxia-associated genes (SOD2, BNIP3, and HMOX1). Our RNA sequencing results were supported by the visual identification of two of those proteins (TLR4 and PTGS2) in the immunohistochemistry analysis. Functional annotation revealed significant enrichment between the DEGs and the toll receptor signaling pathway, which may be a key factor negatively affecting placental functions. In conclusion, our study revealed that the amniotic membrane is not only a physical barrier but also plays an active role in immune response during ascending placentitis.
© 2025. The Author(s).
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Publication Date: 2025-08-21 PubMed ID: 40841585PubMed Central: PMC12371064DOI: 10.1038/s41598-025-16671-5Google Scholar: Lookup
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  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

Overview

  • This research investigates how the gene expression in the equine amniotic membrane changes during ascending placentitis, a bacterial infection that affects the placenta and can result in pregnancy complications like abortion and stillbirth.
  • The study uses RNA sequencing and immunohistochemistry to identify key molecular pathways involved in the disease response, suggesting that the amniotic membrane actively participates in immune defense rather than just serving as a physical barrier.

Background and Importance

  • The amniotic membrane is a critical fetal-maternal tissue that protects the fetus during pregnancy.
  • Despite its importance, the molecular responses of the amniotic membrane during disease states, such as placentitis, are not well understood.
  • Equine ascending placentitis is an infection that ascends from the cervix to infect the placenta, jeopardizing fetal health and possibly causing abortion, preterm birth, or stillbirth.
  • Surfactants produced partly by the amniotic membrane are essential for fetal lung development; disruptions can lead to neonatal complications.
  • Understanding the molecular changes in amniotic membrane during placentitis could help clarify disease mechanisms and inform interventions to prevent adverse pregnancy outcomes.

Study Design and Methods

  • Sample: Pregnant mares were divided into two groups—placentitis (n=6) and control (n=6), matched by gestational age (288 days).
  • Experimental induction of ascending placentitis was performed to simulate natural disease conditions.
  • RNA sequencing (RNA-seq) was used to profile gene expression in the amniotic membranes of infected versus control animals.
  • Bioinformatic analysis identified genes with significant differential expression between placentitis and control groups.
  • Immunohistochemistry validated the protein expression of key genes identified by RNA-seq, focusing on TLR4 and PTGS2.
  • Functional annotation and pathway enrichment analyses were conducted to interpret biological processes involved.

Key Findings

  • 288 genes were found to be differentially expressed in placentitis compared to controls.
  • Upregulated genes included:
    • Toll-like receptor 4 (TLR4), a key receptor involved in the immune response to bacterial infection.
    • Prostaglandin synthesis enzymes PTGS2 (COX-2) and PTGES, which play roles in inflammation and labor induction.
    • Apoptosis-related genes such as MMP9 (matrix metalloproteinase 9) and CASP3 (caspase 3), indicating tissue remodeling and cell death.
    • Hypoxia-associated genes including SOD2 (superoxide dismutase 2), BNIP3, and HMOX1 (heme oxygenase 1), suggesting oxygen deprivation stress during infection.
  • Immunohistochemistry confirmed increased presence of TLR4 and PTGS2 proteins in the amniotic membrane of infected mares, supporting transcriptomic data.
  • Functional enrichment analysis highlighted the toll-like receptor signaling pathway as significantly activated in placentitis, implicating it in placental dysfunction and immune activation.

Implications of the Study

  • The amniotic membrane is not just a passive physical barrier but actively engages in immune defense mechanisms during ascending placentitis.
  • Activation of toll-like receptor signaling suggests the amniotic membrane detects bacterial infection and triggers inflammatory pathways that could contribute to adverse pregnancy outcomes.
  • The involvement of prostaglandin synthesis and apoptotic pathways indicates possible mechanisms by which placentitis may lead to premature labor or fetal loss.
  • Hypoxia-related gene activation points to stress conditions in the placenta during infection, possibly exacerbating tissue damage.
  • These findings could help identify molecular targets for therapeutic intervention and improve management of equine placentitis to reduce fetal complications.

Conclusion

  • This study provides the first comprehensive transcriptomic profile of the equine amniotic membrane during ascending placentitis.
  • It reveals that the amniotic membrane actively participates in immune responses through toll-like receptor signaling and other pathways.
  • Understanding these molecular changes enhances knowledge of the pathophysiology of placentitis and opens avenues for developing strategies to protect fetal health during infection.

Cite This Article

APA
Marchio SP, El-Sheikh Ali H, Scott MA, Barbosa Fernandes C, Scoggin KE, Troedsson M, Boakari Y. (2025). Decoding the amniotic membrane transcriptome during equine ascending placentitis. Sci Rep, 15(1), 30714. https://doi.org/10.1038/s41598-025-16671-5

Publication

Scientific reports
ISSN: 2045-2322
NlmUniqueID: 101563288
Country: England
Language: English
Volume: 15
Issue: 1
Pages: 30714
PII: 30714

Researcher Affiliations

Marchio, Sophia P
  • College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA.
El-Sheikh Ali, Hossam
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, KY, USA.
Scott, Matthew A
  • Veterinary Education, Research, and Outreach Center, Texas A&M University, Canyon, TX, USA.
Barbosa Fernandes, Claudia
  • Department of Animal Reproduction and Veterinary Radiology, School of Veterinary Medicine and Animal Science, University of São Paulo, São Paulo, SP, Brazil.
Scoggin, Kirsten E
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, KY, USA.
Troedsson, Mats
  • Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, University of Kentucky, Lexington, KY, USA.
Boakari, Yatta
  • College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA. yboakari@cvm.tamu.edu.

MeSH Terms

  • Animals
  • Female
  • Horses
  • Amnion / metabolism
  • Amnion / pathology
  • Pregnancy
  • Transcriptome
  • Horse Diseases / genetics
  • Horse Diseases / metabolism
  • Horse Diseases / pathology
  • Placenta Diseases / veterinary
  • Placenta Diseases / genetics
  • Placenta Diseases / metabolism
  • Placenta Diseases / pathology
  • Gene Expression Profiling

Grant Funding

  • RGS 23-02 / VLCS Faculty Grant Texas A&M University

Conflict of Interest Statement

Declarations. Competing interests: The authors declare no competing interests. Ethical approval: This study was approved by IACUC protocol number 2014-1341.

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Citations

This article has been cited 1 times.
  1. Scoggin KE, Rakha SI, Abdellatif AM, Adlan F, Helmy YA, Ruby R, Ball B, Boakari Y, Ali HE. Activation of the S100A8/A9 Alarmin Amplifies Inflammatory Pathways in Equine Ascending Placentitis. Int J Mol Sci 2026 Feb 4;27(3).
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