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[The role of insulin-like growth factor-2 gene differentially methylated regions in TCDD-induced malformation]

Jun Wang1, Yan-yan Zhao, Hong Liu

  • 1Department of Medical Genetics, China Medical University, Shenyang, Liaoning, 110001 PR China.

Zhonghua Yi Xue Yi Chuan Xue Za Zhi = Zhonghua Yixue Yichuanxue Zazhi = Chinese Journal of Medical Genetics
|April 5, 2007
PubMed
Abstract

Insights

Exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) during pregnancy caused fetal rat death, malformations, and growth retardation. These developmental issues may stem from altered insulin-like growth factor 2 (Igf2) gene methylation and expression.

Area of Science:

  • Developmental toxicology
  • Epigenetics
  • Molecular biology

Background:

  • 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a potent environmental toxicant.
  • Insulin-like growth factor 2 (Igf2) plays a crucial role in fetal development.
  • Epigenetic modifications, such as DNA methylation, can influence gene expression and development.

Purpose of the Study:

  • To investigate the impact of TCDD exposure on fetal rat development.
  • To examine the relationship between TCDD-induced developmental abnormalities and Igf2 gene expression and methylation.
  • To explore the role of Igf2 differentially methylated regions (DMRs) in TCDD toxicity.

Main Methods:

  • Pregnant rats were administered a single dose of TCDD on gestation day 10.
  • Fetal development parameters (crown-rump length, body weight, placental weight) were assessed on gestation day 20.
  • Igf2 mRNA and protein levels in fetal liver were quantified using RT-PCR and Western blot.
  • DNA methylation status of Igf2 DMRs in fetal liver was analyzed using methylation-sensitive restriction enzyme PCR and bisulfite sequencing.

Main Results:

  • TCDD exposure resulted in fetal death, absorption, malformations, and significantly reduced growth parameters.
  • Igf2 mRNA and protein expression were significantly upregulated in TCDD-exposed fetal livers.
  • No significant difference in Igf2 DMR1 methylation was observed between groups.
  • Igf2 DMR2 was significantly hypomethylated in TCDD-exposed fetal livers compared to controls.

Conclusions:

  • TCDD exposure during pregnancy induces adverse fetal outcomes, including intrauterine growth retardation (IUGR).
  • TCDD-induced abnormal fetal development in rats is associated with hypomethylation of Igf2 DMR2 and subsequent upregulation of Igf2.
  • These findings highlight the role of epigenetic dysregulation of Igf2 in TCDD-induced developmental toxicity.

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