ArticleBirth defects research2025
Maternal Immune Stimulation With Interferon-Gamma Limits Embryonic Valproic Acid Induced Apoptotic Gene Expression.
Article in Birth defects research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Maternal Immune Stimulation With Interferon-Gamma Limits Embryonic Valproic Acid Induced Apoptotic Gene Expression.Birth defects research · 2025Article
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4 authors.
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Abstract
backgroundNeural tube defects (NTDs) are developmental malformations affecting 1300 newborns in the United States each year. Valproic acid (VA), a drug to treat seizures and mood disorders, can cause NTDs. Apoptosis is increased in the developing neural tubes (NTs) of embryos exposed to VA thereby identifying a possible mechanism for NTD formation. Numerous studies show that maternal immune stimulation (MIS) in the periconceptual period reduces birth defects including VA-induced NTDs. It is hypothesized that immunoregulatory cytokines may normalize the dysregulated apoptosis. This study examined maternal cytokine production and embryonic apoptotic gene expression following prebreeding stimulation with interferon-γ (IFN-γ) and gestational VA exposure.
methodsConcentrations of granulocyte monocyte colony stimulating factor (GM-CSF), IFN-γ, interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-α (TNFα) were determined in VA + IFN-γ-treated pregnant mice. Expression of pro-apoptotic and antiapoptotic pathway genes was determined in VA and VA + IFN-γ exposed embryos.
resultsNTDs decreased from 45.3% to 21.2% per litter with MIS. MIS altered the profiles of GM-CSF and IFN-γ throughout pregnancy and altered the profiles of GM-CSF, IL-6, and IL-10 over the time of NT closure. Pro-apoptotic genes were upregulated, and anti-apoptotic genes were downregulated in VA-exposed embryonic heads with open or closed NTs. Gene expression was normalized with VA + IFN-γ in embryonic heads with closed NTs.
conclusionThis study identified GM-CSF and IFN-γ as possible effectors of MIS and specifically GM-CSF, IL-6, and IL-10 in preventing NTDs. MIS normalized apoptotic gene expression in embryos with closed NTs identifying a possible molecular mechanism for the prevention of VA-induced NTDs.
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