| First Author | Wang F | Year | 2013 |
| Journal | Am J Obstet Gynecol | Volume | 209 |
| Issue | 4 | Pages | 345.e1-7 |
| PubMed ID | 23791840 | Mgi Jnum | J:319472 |
| Mgi Id | MGI:6862344 | Doi | 10.1016/j.ajog.2013.06.037 |
| Citation | Wang F, et al. (2013) Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy. Am J Obstet Gynecol 209(4):345.e1-7 |
| abstractText | 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 2alpha (eIF2alpha), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1alpha (IRE1alpha), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing. RESULTS: Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2alpha, p-PERK, and p-IRE1alpha; 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. |
