Application of iTRAQ proteomics in identification of the differentially expressed proteins of placenta of pregnancy with preeclampsia.

Objective: To explore the differential protein profile of preeclampsia and identify its potential biomarker.

Methods: Around 20 pregnant women with preeclampsia (preeclampsia group) and 20 normal-term pregnancy (normal group) were collected from 2017 to 2018 in the study. Total protein of placenta tissues was extracted, denaturized, deoxidized, and enzymolyzed.

miR-362-3p regulates cell proliferation, migration and invasion of trophoblastic cells under hypoxia through targeting Pax3.

Preeclampsia (PE), a common obstetrical disorder, is one of the leading causes of pregnancy associated death. PE is closely linked with impaired migration and invasion ability of trophoblastic cells. miR-362-3p recently received our particular attention due not only to its aberrant expression in the placentas of patients with PE, but also to its important roles in regulating migration and invasion of various cells.

Alpha-1-antitrypsin functions as a protective factor in preeclampsia through activating Smad2 and inhibitor of DNA binding 4.

Pre-eclampsia (PE) is one of the most common reason for high morbidity and mortality of maternal and prenatal infants. Production from oxidative stress results in maternal ROS system and anti-oxidation defense system imbalance to promote tissue ischemia and hypoxia, and ultimately impairs the maternal organs and placenta. Our previous study showed that exogenous Alpha-1-antitrypsin (AAT) and overexpression of AAT in umbilical vein cell (HUVEC) hypoxia-reoxygenation model could increase the activity of antioxidant enzymes, and played a protective role in preeclampsia animal model.

Metformin ameliorates high uric acid-induced insulin resistance in skeletal muscle cells.

Hyperuricemia occurs together with abnormal glucose metabolism and insulin resistance. Skeletal muscle is an important organ of glucose uptake, disposal, and storage. Metformin activates adenosine monophosphate-activated protein kinase (AMPK) to regulate insulin signaling and promote the translocation of glucose transporter type 4 (GLUT4), thereby stimulating glucose uptake to maintain energy balance.