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Related Experiment Videos

Trichloroethylene effects on gene expression during cardiac development.

J Michael Collier1, Ornella Selmin, Paula D Johnson

  • 1Life Science Division, Genome Sciences, Ernest Orlando Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. mcollier@lbl.gov

Birth Defects Research. Part A, Clinical and Molecular Teratology
|October 21, 2003
PubMed
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Trichloroethylene (TCE) exposure alters gene expression in embryonic rat hearts, down-regulating key developmental genes and up-regulating stress response genes. Serca-2 Ca(2+)-ATPase and GPI-p137 may serve as fetal TCE exposure biomarkers.

Area of Science:

  • Environmental Toxicology
  • Developmental Biology
  • Molecular Biology

Background:

  • Halogenated hydrocarbon exposure, including trichloroethylene (TCE), is linked to altered gene expression in both adult and embryonic tissues.
  • This study investigated differential mRNA transcript expression in embryonic rat hearts following exposure to TCE and its metabolites, dichloroethylene (DCE) and trichloroacetic acid (TCAA).

Purpose of the Study:

  • To identify differentially expressed mRNA transcripts in embryonic rat hearts exposed to TCE, DCE, and TCAA.
  • To investigate potential biomarkers for fetal TCE exposure.

Main Methods:

  • Utilized cDNA subtractive hybridization to amplify mRNA from control and exposed rat embryos.
  • Administered varying doses of TCE, DCE, and TCAA to Sprague-Dawley rats during embryonic development.

Related Experiment Videos

  • Confirmed differential gene expression using dot blot analysis and semi-quantitative RT-PCR.

    • Main Results:

    • Identified numerous differentially regulated gene sequences, including up-regulated stress response (Hsp 70) and homeostasis (ribosomal proteins) genes.
    • Observed down-regulation of extracellular matrix components (GPI-p137, vimentin) and Ca(2+) responsive proteins (Serca-2 Ca(2+)-ATPase, beta-catenin).
    • Identified Serca-2 Ca(2+)-ATPase and GPI-p137 as potential biomarkers for fetal TCE exposure, with decreased expression observed at low TCE levels (100-250 ppb).

    Conclusions:

    • TCE exposure down-regulates genes involved in cellular housekeeping, cell adhesion, and development.
    • TCE exposure up-regulates genes associated with stress response and homeostasis.
    • Serca-2 Ca(2+)-ATPase and GPI-p137 show promise as indicators of fetal TCE exposure.