Placental Glycoredox Dysregulation Associated with Disease Progression in an Animal Model of Superimposed Preeclampsia.

摘要: Pregnancies carried by women with chronic hypertension are at increased risk of superimposed preeclampsia, but the placental pathways involved in disease progression remain poorly understood. In this study, we used stroke-prone spontaneously hypertensive rat (SHRSP) model to investigate mechanisms promoting focus on cellular stress and its influence galectin-glycan circuits. Our analysis revealed that SHRSP placentas characterized a sustained activation response, displaying significantly levels markers lipid peroxidation (i.e., thiobarbituric acid reactive substances (TBARS)) protein nitration defective antioxidant enzyme expression as early gestation day 14 (which marks onset). Further, lectin profiling showed such redox imbalance was associated marked alterations glycocode, including prominent decrease core 1 O-glycan trophoblasts decidual sialylation placentas. We also observed significant changes galectins 1, 3 9 pregnancy progression, highlighting important role galectin signature dynamic interpreters microenvironmental challenges. Collectively, our findings uncover new for glycoredox balance pathogenesis preeclampsia representing promising target interventions disorders pregnancy.