Purpose of Review
Preeclampsia (PE) is a leading global cause of maternal and fetal morbidity and mortality. The heterogeneity of this disorder contributes to its elusive etiology. Due to the ethical constraints surrounding human studies, animal models provide a suitable alternative for investigation into PE pathogenesis and novel therapeutic strategies. The purpose of this review is to compare and contrast the various rodent models used to study PE, in order to demonstrate their value in investigating and identifying different characteristics of this disorder.
Recent Findings
Several approaches have been employed to create an appropriate animal model of PE, including surgical, genetic manipulation, and pharmacological methods in an attempt to mimic the maternal syndrome. Despite the absence of a model to completely model PE, these models have provided valuable information concerning various aspects of PE pathogenesis and novel therapeutic strategies and have led to the discovery of potential predictive markers of PE.
Summary
Rodent and murine models have contributed significantly to the study of the pathology associated with specific aspects of the disorder. As a single fully encompassing animal model of PE remains absent, the use of a combination of models has potential value in understanding its etiology as well as in new treatment and management strategies.
Objective: Approximately 30% of preeclamptic pregnancies exhibit abnormal liver function tests. We assessed liver injury-associated enzyme levels and circulating transforming growth factor beta (TGF-β) levels in an arginine vasopressin (AVP)-induced pregnant Sprague-Dawley rat model.Methods: Pregnant and non-pregnant Sprague-Dawley rats (n=24) received AVP (150 ng/hr) subcutaneously via mini-osmotic pumps for 18 days. Blood pressure was measured, urine samples were collected, and all animals were euthanized via isoflurane. Blood was collected to measure circulating levels of TGF-β1-3 isomers and liver injury enzymes in pregnant AVP (PAVP), pregnant saline (PS), non-pregnant AVP (NAVP), and non-pregnant saline (NS) rats. Results: The PAVP group showed significantly higher systolic and diastolic blood pressure than both saline-treated groups. The weight per pup was significantly lower in the AVP-treated group than in the saline group (p<0.05). Circulating TGF-β1-3 isomer levels were significantly higher in the PAVP rats than in the NS rats. However, similar TGF-1 and TGF-3 levels were noted in the PS and PAVP rats, while TGF-2 levels were significantly higher in the PAVP rats. Circulating liver-type arginase-1 and 5'-nucleotidase levels were higher in the PAVP rats than in the saline group. Conclusion: This is the first study to demonstrate higher levels of TGF-β2, arginase, and 5'-nucleotidase activity in PAVP than in PS rats. AVP may cause vasoconstriction and increase peripheral resistance and blood pressure, thereby elevating TGF-β and inducing the preeclampsia-associated inflammatory response. Future studies should explore the mechanisms through which AVP dysregulates liver injury enzymes and TGF-β in pregnant rats.
Objectives: To establish the circulating levels of copeptin and fibronectin in normal and preeclamptic Black South African pregnant females. Materials and Methods: Serum copeptin and fibronectin levels were measured in preeclamptic and normotensive women via enzyme-linked immunosorbent assays. Data are presented as medians and interquartile ranges. Spearman's chi-square test was used to evaluate bivariate associations between analytes and clinical variables. Results: Fibronectin levels were downregulated in preeclampsia (PE) compared to the control group (P < 0.05). Copeptin levels displayed an upward trend in PE compared to the normotensive group. Blood pressure (systolic and diastolic) was significantly different between preeclamptic and normotensive women (P < 0.005). In the preeclamptic group, gestational age was negatively correlated with systolic blood pressure (r = -0.8, P < 0.05). In addition, diastolic blood pressure was negatively correlated with maternal weight (r=-0.58, P < 0.05) and gestational age (r = -0.76, P < 0.05) in the preeclamptic group. Eventually, a positive correlation was noted between diastolic blood pressure and systolic blood pressure (r = 0.65, P < 0.05) in PE. Conclusions: This was the first South African study to measure copeptin and fibronectin in pregnant women. The findings demonstrated a dysregulation in copeptin and fibronectin serum levels between the normotensive pregnant and preeclamptic groups, suggesting a potential diagnostic indicator of PE development.
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