Evidence map›Paper›PMID 20457659›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2010

Genetic and maternal effects on valproic acid teratogenesis in C57BL/6J and DBA/2J mice.

Chris Downing, Jami Biers, Colin Larson, Alexi Kimball, Hali Wright, Takamasa Ishii, David Gilliam, Thomas Johnson

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

9 citing papers in PubMed, 28 citations in OpenAlex.

  1. Association of UGT2B7 and UGT1A4 Polymorphisms with Serum Concentration of Antiepileptic Drugs in Children.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Tissue-specific effects of valproic acid on DNA repair genes and apoptosis in postimplantation mouse embryos.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  7. Article
  8. Article
  9. The role of neuronal apoptosis in Valproic Acid brain-related teratogenesis: a histochemical and immunohistochemical study in BALB/c mice.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

8 authors at 2 institutions in 1 country.

Chris DowningInstitute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309-0447, USA. cdowning@pharmacy.isu.edu
Jami Biers
Colin Larson
Alexi Kimball
Hali Wright
Takamasa Ishii
David Gilliam
Thomas Johnson
University of Colorado Boulder · USUniversity of Northern Colorado · US

Funding

Ethanol Teratogenesis and Genomic ImprintingR01AA016676 · NIAAA · UNIVERSITY OF COLORADO · PI JOHNSON, THOMAS E. · 2006 to 2010
$2.1M
NIAAA NIH HHS R01AA016676NIAAA NIH HHS R24 AA01466
6 · The paper itself

Abstract

Valproic acid (VPA) is used worldwide to treat epilepsy, migraine headaches, and bipolar disorder. However, VPA is teratogenic and in utero exposure can lead to congenital malformations. Using inbred C57BL/6J (B6) and DBA/2J (D2) mice, we asked whether genetic variation could play a role in susceptibility to VPA teratogenesis. Whereas B6 fetuses were more susceptible than D2 fetuses to digit and vertebral malformations, D2 fetuses were more susceptible to rib malformations. In a reciprocal cross between B6 and D2, genetically identical F1 mice carried in a B6 mother had a greater percentage of vertebral malformations following prenatal VPA exposure than F1 mice carried in a D2 mother. This reciprocal F1 difference is known as a maternal effect and shows that maternal genotype/uterine environment is an important mediator of VPA teratogenecity. VPA is a histone deacetylase inhibitor, and it is possible that the differential teratogenesis in B6 and D2 is because of strain differences in histone acetylation. We observed strain differences in acetylation of histones H3 and H4 in both embryo and placenta following in utero VPA exposure, but additional studies are needed to determine the significance of these changes in mediating teratogenesis. Our results provide additional support that genetic factors, both maternal and fetal, play a role in VPA teratogenesis. Lines of mice derived from B6 and D2 will be a useful model for elucidating the genetic architecture underlying susceptibility to VPA teratogenesis.

Indexed as

Abnormalities, Drug-InducedAnimalsAnticonvulsantsBlotting, WesternDose-Response Relationship, DrugFemaleGenotypeHistone Deacetylase InhibitorsHistone DeacetylasesMaleMiceMice, Inbred C57BLMice, Inbred DBASpecies SpecificityValproic AcidAnticonvulsantsHistone Deacetylase InhibitorsHistone DeacetylasesValproic Acid

Identifiers

PMID20457659
PMCPMC2905403
OpenAlexW2130530931

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.