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Related Experiment Video

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Analysis of Retinoic Acid-induced Neural Differentiation of Mouse Embryonic Stem Cells in Two and Three-dimensional Embryoid Bodies
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Transcriptomic changes in mouse embryonic stem cells exposed to thalidomide during spontaneous differentiation.

Xiugong Gao1, Robert L Sprando1, Jeffrey J Yourick1

  • 1Division of Toxicology, Office of Applied Research and Safety Assessment, Center for Food Safety and Applied Nutrition, U.S. Food and Drug Administration, Laurel, MD, USA.

Data in Brief
|July 29, 2015
PubMed
Summary

Thalidomide causes birth defects by disrupting gene expression. This study used mouse embryonic stem cells (mESCs) to identify early molecular changes linked to thalidomide embryopathy.

Keywords:
Developmental toxicityDifferentiationEmbryonic stem cellMicroarrayMouseThalidomideTranscriptomics

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Area of Science:

  • Developmental toxicology
  • Molecular biology
  • Stem cell research

Background:

  • Thalidomide is a known teratogen causing severe birth defects, particularly limb malformations.
  • The precise molecular mechanisms underlying thalidomide's teratogenic effects remain incompletely understood.
  • Understanding these mechanisms is crucial for preventing developmental abnormalities.

Purpose of the Study:

  • To investigate the early transcriptomic changes induced by thalidomide exposure in a relevant in vitro model.
  • To identify key molecular pathways perturbed by thalidomide during early embryonic development.
  • To provide complementary data for a previously published study on thalidomide-induced gene expression changes.

Main Methods:

  • Utilized microarray analysis to profile gene expression in differentiating mouse embryonic stem cells (mESCs).
  • Exposed mESCs to thalidomide during critical differentiation stages.
  • Analyzed transcriptomic data to identify differentially expressed genes and pathways.

Main Results:

  • Thalidomide exposure led to significant perturbations in early gene expression patterns in mESCs.
  • Identified specific gene sets and molecular pathways affected by thalidomide, indicative of potential human embryopathy.
  • The observed transcriptomic changes provide insights into the molecular basis of thalidomide teratogenicity.

Conclusions:

  • Early gene expression alterations in mESCs serve as a sensitive indicator of thalidomide's developmental toxicity.
  • The findings contribute to a deeper understanding of thalidomide's teratogenic mechanisms at the molecular level.
  • This research supports the use of mESC models for studying drug-induced developmental toxicity.