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Apoptosis and its pathway in early post-implantation embryos of diabetic rats

Fuyan Sun1, Eiji Kawasaki, Shoichi Akazawa

  • 1Department of Metabolism/Diabetes and Clinical Nutrition, Nagasaki University Hospital of Medicine and Dentistry, Nagasaki, Japan.

Diabetes Research and Clinical Practice
|January 15, 2005
PubMed

Insights

Diabetes during pregnancy can cause neural tube defects by increasing embryonic cell death. This study reveals that a specific protein pathway involving Bax and caspase-3 activation contributes to this increased apoptosis in diabetic rat embryos.

Area of Science:

  • Developmental biology
  • Cell biology
  • Toxicology

Background:

  • Diabetes mellitus is a risk factor for congenital anomalies.
  • Embryonic apoptosis during neurulation is implicated in neural tube defects.

Purpose of the Study:

  • To investigate apoptosis and its molecular pathways in early post-implantation embryos from diabetic rats.
  • To determine the role of Bax, Bcl-2, and caspase-3 in diabetic embryopathy.

Main Methods:

  • Streptozotocin (STZ)-induced diabetes in rats.
  • Quantitative RT-PCR to analyze gene expression (bax, bcl-2).
  • Terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) assay for apoptosis.
  • Immunohistochemistry for Bax, activated caspase-3, and Bcl-2.

Main Results:

  • Significantly decreased bcl-2 mRNA expression in diabetic rat embryos.
  • Increased number of TUNEL-positive cells, particularly in the primitive brain, of diabetic embryos.
  • Upregulation of Bax and activated caspase-3, with low Bcl-2 expression in apoptotic cells of diabetic embryos.

Conclusions:

  • A Bax-regulated mitochondrial pathway involving cytochrome c and caspase-3 activation is likely implicated in diabetic embryopathy.
  • This pathway contributes to inappropriate apoptosis in embryos exposed to diabetes, potentially leading to neural tube defects.

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