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Reliability of Rodent and Rabbit Models in Preeclampsia Research

Journal

Publisher

MDPI
DOI: 10.3390/ijms232214344

Keywords

mouse; placenta; preeclampsia; rabbit; rat; rodents; trophoblast

Funding

  1. Medical University of Lodz [503/0-07801/503-01-001-19-00]

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In vivo studies on gestational pathology often use small mammals as models due to their similarities to humans in terms of reproductive cycle and placental development. However, there are differences in the process of vessel remodeling and trophoblast invasion between these animals and humans, limiting their use in studying preeclampsia.
In vivo studies on the pathology of gestation, including preeclampsia, often use small mammals such as rabbits or rodents, i.e., mice, rats, hamsters, and guinea pigs. The key advantage of these animals is their short reproductive cycle; in addition, similar to humans, they also develop a haemochorial placenta and present a similar transformation of maternal spiral arteries. Interestingly, pregnant dams also demonstrate a similar reaction to inflammatory factors and placentally derived antiangiogenic factors, i.e., soluble fms-like tyrosine kinase 1 (sFlt-1) or soluble endoglin-1 (sEng), as preeclamptic women: all animals present an increase in blood pressure and usually proteinuria. These constitute the classical duet that allows for the recognition of preeclampsia. However, the time of initiation of maternal vessel remodelling and the depth of trophoblast invasion differs between rabbits, rodents, and humans. Unfortunately, at present, no known animal replicates a human pregnancy exactly, and hence, the use of rabbit and rodent models is restricted to the investigation of individual aspects of human gestation only. This article compares the process of placentation in rodents, rabbits, and humans, which should be considered when planning experiments on preeclampsia; these aspects might determine the success, or failure, of the study. The report also reviews the rodent and rabbit models used to investigate certain aspects of the pathomechanism of human preeclampsia, especially those related to incorrect trophoblast invasion, placental hypoxia, inflammation, or maternal endothelial dysfunction.

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