Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Type of study
Language
Publication year range
1.
Toxicol Appl Pharmacol ; 275(2): 134-44, 2014 Mar 01.
Article in English | MEDLINE | ID: mdl-24370435

ABSTRACT

The role of endoplasmic reticulum (ER) stress in pregnancy remains largely unknown. Pregnant mice were subcutaneously administered tunicamycin (Tun), an ER stressor, as a single dose [0, 50, and 100 µg Tun/kg/body weight (BW)] on gestation days (GDs) 8.5, 12.5, and 15.5. A high incidence (75%) of preterm delivery was observed only in the group treated with Tun 100 µg/kg BW at GD 15.5, indicating that pregnant mice during late gestation are more susceptible to ER stress on preterm delivery. We further examined whether prolonged in utero exposure to ER stress affects fetal development. Pregnant mice were subcutaneously administered a dose of 0, 20, 40, and 60 µg Tun/kg from GD 12.5 to 16.5. Tun treatment decreased the placental and fetal weights in a dose-dependent manner. Histological evaluation showed the formation of a cluster of spongiotrophoblast cells in the labyrinth zone of the placenta of Tun-treated mice. The glycogen content of the fetal liver and placenta from Tun-treated mice was lower than that from control mice. Tun treatment decreased mRNA expression of Slc2a1/glucose transporter 1 (GLUT1), which is a major transporter for glucose, but increased placental mRNA levels of Slc2a3/GLUT3. Moreover, maternal exposure to Tun resulted in a decrease in vascular endothelial growth factor receptor-1 (VEGFR-1), VEGFR-2, and placental growth factor. These results suggest that excessive and exogenous ER stress may induce functional abnormalities in the placenta, at least in part, with altered GLUT and vascular-related gene expression, resulting in low infant birth weight.


Subject(s)
Endoplasmic Reticulum Stress/drug effects , Infant, Low Birth Weight , Placenta/drug effects , Stress, Physiological/drug effects , Animals , Female , Fetal Development/drug effects , Fetal Growth Retardation/chemically induced , Fetal Growth Retardation/physiopathology , Fetal Weight/drug effects , Glucose Transporter Type 1/genetics , Glucose Transporter Type 1/metabolism , Glucose Transporter Type 3/genetics , Glucose Transporter Type 3/metabolism , Male , Maternal Exposure , Mice , Mice, Inbred ICR , Placenta/physiopathology , Pregnancy , RNA, Messenger/genetics , RNA, Messenger/metabolism , Transcription Factor CHOP/genetics , Transcription Factor CHOP/metabolism , Tunicamycin/administration & dosage , Tunicamycin/adverse effects , Vascular Endothelial Growth Factor Receptor-1/genetics , Vascular Endothelial Growth Factor Receptor-1/metabolism , Vascular Endothelial Growth Factor Receptor-2/genetics , Vascular Endothelial Growth Factor Receptor-2/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL
...