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Oxidative stress in diabetic pregnancy alters gene expression and apoptosis leading to congenital heart defects in embryos
Author(s) -
Kumar S.D.,
Cheng Y.J.,
Lo S.L.,
Kang Y.J.,
Bay B.H.,
Tay S.S.W.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.642.2
Subject(s) - oxidative stress , sod2 , malondialdehyde , andrology , apoptosis , downregulation and upregulation , diabetes mellitus , embryo , endocrinology , medicine , biology , gene , microbiology and biotechnology , superoxide dismutase , genetics
Congenital heart defects are frequently present in infants of diabetic mothers. The present study investigated the role of oxidative stress in the developing hearts of embryos from diabetic mothers. SuperArray analysis showed significant alterations of metabolic oxidative stress‐related genes (Gpx3, Fancc, Hbq1, Il22, Nqo1, Sod2 and Tmod1) in the hearts of experimental embryos. Further, the lipid hydroperoxidation level was significantly upregulated in the developing hearts of embryos from diabetic mothers. Western blot confirmed that the protein level of malondialdehyde (MDA) was significantly upregulated in the defective hearts. In addition, MTS assay was performed to assess the viability of H9C2 cell line (cardiomyoblasts) exposed to different glucose concentrations at various time points. Cell viability was significantly decreased in cardiomyoblast cultures treated with high glucose concentrations at all time points studied. Transmission electron microscopy confirmed that apoptotic cell death was upregulated in cardiomyoblasts exposed to high glucose concentrations. It is hypothesized that oxidative stress from maternal diabetes alters the expressions of genes and apoptosis which are involved in the development of the heart, thereby contributing to congenital heart defects. Supported by grants R‐181‐000‐101‐112 & R‐181‐000‐117‐101 from National University of Singapore. Grant Funding Source AAA Postdoctoral Travel Award & AAA Postdoctoral Fellow Poster Presentation Award