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Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy.

Abstract：

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 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing. RESULTS:Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; 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.

journal_name

Am J Obstet Gynecol

journal_title

American journal of obstetrics and gynecology

authors

Wang F,Reece EA,Yang P

doi

10.1016/j.ajog.2013.06.037

keywords:

["diabetic embryopathy","endoplasmic reticulum stress","oxidative stress","superoxide dismutase 1 transgenic mice"]

subject

Has Abstract

pub_date

2013-10-01 00:00:00

pages

345.e1-7

issue

4

eissn

0002-9378

issn

1097-6868

pii

S0002-9378(13)00653-4

journal_volume

209

pub_type

杂志文章

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