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Diabetes and apoptosis: neural crest cells and neural tube

James H Chappell1, Xiao Dan Wang, Mary R Loeken

  • 1Section on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA. james.chappell@joslin.harvard.edu

Apoptosis : an International Journal on Programmed Cell Death
|April 1, 2009
PubMed

Insights

Diabetic pregnancy can cause birth defects by triggering progenitor cell death. Maternal diabetes reduces Pax3 gene expression, leading to apoptosis and developmental abnormalities like cardiac and neural tube defects.

Area of Science:

  • Developmental biology
  • Genetics
  • Teratology

Background:

  • Diabetic pregnancy is a known risk factor for congenital birth defects.
  • These defects arise from the apoptosis (programmed cell death) of essential progenitor cells during organogenesis.
  • Insufficient gene expression regulating cell viability is implicated in this process.

Purpose of the Study:

  • To investigate the molecular mechanisms linking diabetic pregnancy to birth defects.
  • To identify specific genes and cellular pathways involved in progenitor cell apoptosis.
  • To provide a cellular explanation for cardiac outflow tract and neural tube defects.

Main Methods:

  • Analysis of gene expression in the context of maternal diabetes.
  • Focus on the role of the Pax3 transcription factor.
  • Investigation of the p53 tumor suppressor protein pathway in neural crest and neuroepithelial cells.

Main Results:

  • Maternal diabetes was found to inhibit the expression of the Pax3 gene.
  • Insufficient Pax3 leads to apoptosis of cardiac neural crest and neuroepithelial cells.
  • This apoptosis is dependent on the p53 tumor suppressor protein.

Conclusions:

  • Reduced Pax3 expression due to maternal diabetes is a key factor in progenitor cell apoptosis.
  • The p53 pathway mediates the apoptotic process in response to insufficient Pax3.
  • This provides a cellular basis for understanding birth defects in diabetic pregnancies.

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