ArticleEnvironmental health perspectives2004
Valproic acid teratogenicity: a toxicogenomics approach.
Article in Environmental health perspectives, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 87 citations in OpenAlex.
- Moringa Oleifera mitigates oxidative stress and pancreatic toxicity induced by sodium valproate in female Sprague Dawley rats.Journal of molecular histology · 2025Article
- Delving into the Complexity of Valproate-Induced Autism Spectrum Disorder: The Use of Zebrafish Models.Cells · 2024Article
- Article
- Valproic Acid in Pregnancy Revisited: Neurobehavioral, Biochemical and Molecular Changes Affecting the Embryo and Fetus in Humans and in Animals: A Narrative Review.International journal of molecular sciences · 2023Review
- Gal-2 Increases H3K4meBiomolecules · 2022Article
- Epidemiology, prenatal management, and prevention of neural tube defects.Saudi medical journal · 2014Review
- Risk factors for neural tube defects in Riyadh City, Saudi Arabia: Case-control study.Sudanese journal of paediatrics · 2014Article
- MicroRNA profiling as tool for in vitro developmental neurotoxicity testing: the case of sodium valproate.PloS one · 2014Article
- A human pluripotent stem cell platform for assessing developmental neural toxicity screening.Stem cell research & therapy · 2013Review
- Effects of lithium and valproic acid on gene expression and phenotypic markers in an NT2 neurosphere model of neural development.PloS one · 2013Article
- Interaction networks of lithium and valproate molecular targets reveal a striking enrichment of apoptosis functional clusters and neurotrophin signaling.The pharmacogenomics journal · 2012Article
- Reduction in valproic acid-induced neural tube defects by maternal immune stimulation: role of apoptosis.Birth defects research. Part B, Developmental and reproductive toxicology · 2012Article
- Ethanol exposure alters protein expression in a mouse model of fetal alcohol spectrum disorders.International journal of proteomics · 2012Article
- Genetic and maternal effects on valproic acid teratogenesis in C57BL/6J and DBA/2J mice.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Ascorbic acid reverses valproic acid-induced inhibition of hoxa2 and maintains glutathione homeostasis in mouse embryos in culture.Cellular and molecular neurobiology · 2010Article
- Metabolomics in the assessment of chemical-induced reproductive and developmental outcomes using non-invasive biological fluids: application to the study of butylbenzyl phthalate.Journal of applied toxicology : JAT · 2009Article
- Expression of homeotic genes Hoxa3, Hoxb3, Hoxd3 and Hoxc4 is decreased in the lungs but not in the hearts of adriamycin-exposed mice.Pediatric surgery international · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Embryonic development is a highly coordinated set of processes that depend on hierarchies of signaling and gene regulatory networks, and the disruption of such networks may underlie many cases of chemically induced birth defects. The antiepileptic drug valproic acid (VPA) is a potent inducer of neural tube defects (NTDs) in human and mouse embryos. As with many other developmental toxicants however, the mechanism of VPA teratogenicity is unknown. Using microarray analysis, we compared the global gene expression responses to VPA in mouse embryos during the critical stages of teratogen action in vivo with those in cultured P19 embryocarcinoma cells in vitro. Among the identified VPA-responsive genes, some have been associated previously with NTDs or VPA effects [vinculin, metallothioneins 1 and 2 (Mt1, Mt2), keratin 1-18 (Krt1-18)], whereas others provide novel putative VPA targets, some of which are associated with processes relevant to neural tube formation and closure [transgelin 2 (Tagln2), thyroid hormone receptor interacting protein 6, galectin-1 (Lgals1), inhibitor of DNA binding 1 (Idb1), fatty acid synthase (Fasn), annexins A5 and A11 (Anxa5, Anxa11)], or with VPA effects or known molecular actions of VPA (Lgals1, Mt1, Mt2, Id1, Fasn, Anxa5, Anxa11, Krt1-18). A subset of genes with a transcriptional response to VPA that is similar in embryos and the cell model can be evaluated as potential biomarkers for VPA-induced teratogenicity that could be exploited directly in P19 cell-based in vitro assays. As several of the identified genes may be activated or repressed through a pathway of histone deacetylase (HDAC) inhibition and specificity protein 1 activation, our data support a role of HDAC as an important molecular target of VPA action in vivo.
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What OpenQuestion holds
Registered trials
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.