Pre-existing or new onset of hypertension affects pregnancy and is one of the leading causes of maternal and fetal morbidity and mortality. In certain cases, it also leads to long… Click to show full abstract
Pre-existing or new onset of hypertension affects pregnancy and is one of the leading causes of maternal and fetal morbidity and mortality. In certain cases, it also leads to long term maternal cardiovascular complications. The placenta is a key player in the pathogenesis of complicated hypertensive pregnancies, however the pathomechanisms leading to an abnormal placenta are poorly understood. In this study we compared the placental proteome of two rat models: a pre-existing hypertension pregnancy model (stroke-prone spontaneously hypertensive, SHRSP) and the transgenic RAS activated gestational hypertension model (transgenic for human angiotensinogen Sprague-Dawley rats, SD-PE). Label-free proteomics using nano LC-MS/MS was performed for identification and quantification of proteins. Between the two models, we found widespread differences in the expression of placental proteins including those related to hypertension, inflammation and trophoblast invasion; whereas pathways such as regulation of serine endopeptidase activity, tissue injury response, coagulation and complement activation were enriched in both models. We present for the first time the placental proteome of SHRSP and SD-PE and provide insight into the molecular make-up of models of hypertensive pregnancy. Our study informs future research into specific preeclampsia and chronic hypertension pregnancy mechanisms and translation of rodent data to the clinic.
               
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