Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-135 |
Sentence |
denotes |
Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy. |
T2 |
136-146 |
Sentence |
denotes |
OBJECTIVE: |
T3 |
147-256 |
Sentence |
denotes |
Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. |
T4 |
257-309 |
Sentence |
denotes |
We tested whether oxidative stress causes ER stress. |
T5 |
310-323 |
Sentence |
denotes |
STUDY DESIGN: |
T6 |
324-883 |
Sentence |
denotes |
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. |
T7 |
884-892 |
Sentence |
denotes |
RESULTS: |
T8 |
893-1098 |
Sentence |
denotes |
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. |
T9 |
1099-1168 |
Sentence |
denotes |
SOD1 overexpression blocked these diabetes-induced ER stress markers. |
T10 |
1169-1180 |
Sentence |
denotes |
CONCLUSION: |
T11 |
1181-1284 |
Sentence |
denotes |
Mitigating oxidative stress via SOD1 overexpression blocks maternal diabetes-induced ER stress in vivo. |