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Updated: May 30, 2026
10:07
Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
Published on: March 20, 2012
Increased hepatic Igf2 gene expression involves C/EBPβ in TCDD-induced teratogenesis in rats
Jun Wang1, Xiaoliang Liu, Tingting Li
1Department of Clinical Genetics, Shengjing Hospital of China Medical University, Shenyang, Liaoning, PR China.
Reproductive Toxicology (Elmsford, N.Y.)
|July 23, 2011
Summary
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure increases Insulin-like growth factor 2 (Igf2) expression in fetal rats. TCDD upregulates CCAAT/enhancer binding protein β (C/EBPβ), enhancing Igf2 gene transcription and potentially causing developmental toxicity.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Molecular Endocrinology
Background:
- 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminant linked to reproductive and developmental toxicity.
- Insulin-like growth factor 2 (Igf2) plays a critical role in regulating fetal growth and development.
Purpose of the Study:
- To investigate the potential role of Igf2 in mediating TCDD-induced developmental toxicity.
- To elucidate the molecular mechanisms by which TCDD affects Igf2 gene expression.
Main Methods:
- Real-time quantitative RT-PCR and Western blotting to assess Igf2 expression.
- Electrophoresis mobility shift assay and chromatin immunoprecipitation to identify transcription factor binding sites.
- Luciferase assay to measure promoter activity.
Main Results:
- TCDD exposure in pregnant rats resulted in fetal growth restriction and malformations.
- TCDD significantly elevated Igf2 mRNA and protein levels in fetal rat liver and BRL-3A cells.
- A CCAAT/enhancer binding protein β (C/EBPβ) binding site in the Igf2 P3-promoter was identified, and TCDD enhanced C/EBPβ binding and Igf2 promoter activity.
Conclusions:
- TCDD induces Igf2 gene expression via C/EBPβ transactivation.
- Upregulation of Igf2 by TCDD may contribute to the observed developmental effects in rats.
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