Abstract
Preeclampsia is hallmarked by systemic endothelial dysfunction, including increased endothelial permeability and oedema. Placenta-derived factors in maternal blood contribute to endothelial barrier impairment, but molecular mechanisms are unclear. HtrA4 is a placenta-specific protease that is secreted into the maternal circulation and elevated in early-onset preeclampsia. In this study, we found HtrA4 cleaved the key endothelial junctional protein VE-cadherin in vitro. HtrA4 at concentrations found in preeclampsia also cleaved VE-cadherin in HUVECs as an endothelial model, disrupted cell-cell connections and induced intercellular gaps. These results provide critical insights into understanding the molecular mechanisms of endothelial barrier disruption in preeclampsia.
Original language | English |
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Pages (from-to) | 51-53 |
Number of pages | 3 |
Journal | Placenta |
Volume | 76 |
Issue number | 15 |
DOIs | |
Publication status | Published - 15 Jan 2019 |
Keywords
- Endothelial barrier
- HtrA4
- Oedema
- Preeclampsia
- Vascular permeability
- VE-Cadherin