Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 209, Issue 4, Pages -Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2013.06.037
Keywords
diabetic embryopathy; endoplasmic reticulum stress; oxidative stress; superoxide dismutase 1 transgenic mice
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Funding
- National Institutes of Health [R01DK083243, R56 DK095380]
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OBJECTIVE: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress. STUDY DESIGN: Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2 alpha (eIF2 alpha), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1 alpha (IRE1 alpha), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing. RESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2 alpha, p-PERK, and p-IRE1 alpha; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers. CONCLUSION: Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo.
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