Missing links in preeclampsia cell model systems of endothelial dysfunction |
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| Affiliation: | 1. Department of Biophysics and Pharmacology, Institute of Biosciences, Sao Paulo State University (UNESP), Botucatu, São Paulo, Brazil;2. Laboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, São Paulo, São Paulo, Brazil;3. European Molecular Biology Laboratory, European Bioinformatics Institute, Hinxton, UK;1. Vall d’Hebron Research Institute (VHIR). Universitat Autónoma de Barcelona, Barcelona, 08035, Spain;2. Instituto de Investigación Sanitaria y Biomédica de Alicante (ISABIAL), Alicante, 03010, Spain;3. Instituto de Neurosciencias CSIC-UMH, San Juan de Alicante, 03550, Spain;1. CNC-Center for Neuroscience and Cell Biology, University of Coimbra, Portugal;2. Centre for Innovation in Biomedicine and Biotechnology (CIBB), University of Coimbra, Portugal;3. Institute for Interdisciplinary Research (IIIUC), University of Coimbra, Coimbra, Portugal;4. Faculty of Pharmacy, University of Coimbra, Portugal;1. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA;2. Department of Psychiatry and Alzheimer’s Disease Research Center, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA;3. James J Peters VA Medical Center, Bronx, NY 10468, USA |
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| Abstract: | Preeclampsia, one of the main hypertensive disorders of pregnancy, is associated with circulating factors released by the ischemic placenta accompanied by systemic endothelial dysfunction. The etiology of preeclampsia remains poorly understood although it is associated with high maternal and fetal mortality and increased cardiovascular disease risk. Most cell model systems used for studying endothelial dysfunction have not taken into account hemodynamic physical factors such as shear-stress forces which may prevent extrapolation of cell data to in vivo settings. We overview the role of hemodynamic forces in modulating endothelial cell function and discuss strategies to reproduce this biological characteristic in vitro to improve our understanding of endothelial dysfunction associated with preeclampsia. |
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