Evidence map›Paper›PMID 40119254›Full record

ArticleBMC genomics2025

Altered structural and transporter-related gene expression patterns in the placenta play a role in fetal demise during Porcine reproductive and respiratory syndrome virus infection.

Angelica Van Goor, Alex Pasternak, Kristen E Walker, Shannon Chick, John C S Harding, Joan K Lunney

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In one paragraph

Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Angelica Van Goor *Animal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, ARS, USDA, Beltsville, MD, USA.
Alex Pasternak *Department of Animal Sciences, Purdue University, West Lafayette, IN, USA.
Kristen E WalkerAnimal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, ARS, USDA, Beltsville, MD, USA.
Shannon ChickAnimal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, ARS, USDA, Beltsville, MD, USA.
John C S HardingDepartment of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Joan K LunneyAnimal Parasitic Diseases Laboratory, Beltsville Agricultural Research Center, ARS, USDA, Beltsville, MD, USA. joan.lunney@usda.gov.

Funding

Agricultural Research Service project 8042-32000-102/117Genome Alberta Administrative supportGenome Canada Project 2014LSARP_8202Genome Prairie Project 346143PigGen Canada Industry support
6 · The paper itself

Abstract

backgroundPorcine reproductive and respiratory syndrome virus (PRRSV) can be transmitted across the maternal-fetal-interface from an infected gilt to her fetuses. Although fetal infection status and disease outcomes vary, the mechanisms are not completely understood. The objective was to assess targeted placental structural and transporter-related gene expression patterns. At day 85 of gestation pregnant pigs were challenged with PRRSV, and at 12 days post maternal infection sows and fetuses were sacrificed, and the placental tissue was collected. Grouping of fetuses was by preservation status and PRRS viral load (VL): control (CTRL, n = 14), viable and low VL fetus (VIA_LVF, n = 15), viable and high VL fetus (VIA_HVF, n = 21), meconium mild and low VL fetus (MECm_LVF, n = 14), meconium mild and high VL fetus (MECm_HVF, n = 14), and meconium severe and high VL fetus (MECs_HVF, n = 13). NanoString was used to evaluate the expression of 86 genes: actin cytoskeleton signaling, arachidonic acid pathway, integrin signaling, intercellular junctions, transporters, and VEGF signaling. Statistical analyses were performed using Limma with P ≤ 0.05 considered significant.

resultsWe identified 1, 7, 0, 29, and 39 differentially expressed genes in VIA_LVF, VIA_HVF, MECm_LVF, MECm_HVF, and MECs_HVF, respectively, contrasted to CTRL. Placental transporter genes were significantly impacted (i.e., downregulation of SLC1A3, SLC1A5, SLC2A1, SLC2A3, SLC2A5, SLC2A10, SLC2A12, SLC7A4, SLC16A5, SLC16A10, and SLC27A6; and upregulation of SLC2A2, SLC16A3, and SLC27A4), compared to CTRL. Actin cytoskeleton signaling (ARHGEF6 and ARHGEF7), arachidonic acid (PTGES3 and PTGIS), integrin signaling (FN1 and ITGB6), intercellular junctions (CDH3 and CDH11), and VEGF signaling (MAPK3 and HPSE) gene groupings were significantly impacted, compared to CTRL.

conclusionData reported here indicate that fetal PRRSV infection levels rather than fetal demise is necessary for transcriptional dysregulation of the fetal placenta, with a tendency towards more downregulation in the target gene sets among susceptible fetuses. These results generally support that in susceptible fetuses there is altered solute transportation, placental structural integrity, and reduced angiogenesis. The data described here is associated with fetal PRRS resistance/resilience and susceptibility.

Indexed as

PlacentaPorcine Reproductive and Respiratory SyndromePorcine respiratory and reproductive syndrome virusAnimalsFemaleFetal DeathFetusGene Expression ProfilingPregnancySwineTranscriptomeAngiogenesisArachidonic acidDisease resistanceFetal pigGene expressionIntercellular junctionsPlacentaPorcine reproductive and respiratory syndromeSolute carrier proteinsStructural pathways

Identifiers

PMID40119254
PMCPMC11927291

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.