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 |
|---|---|
| Number of pages | 3 |
| Journal | Placenta |
| DOIs | |
| Publication status | Accepted/In press - 1 Jan 2019 |
Keywords
- Endothelial barrier
- HtrA4
- Oedema
- Preeclampsia
- Vascular permeability
- VE-Cadherin
Cite this
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Elevated protease HtrA4 in the maternal circulation of preeclampsia may contribute to endothelial barrier disruption by cleaving key junctional protein VE-cadherin. / Tseng, Esther; Yee Teoh, Sonia Soo; Wang, Yao; Nie, Guiying.
In: Placenta, 01.01.2019.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Elevated protease HtrA4 in the maternal circulation of preeclampsia may contribute to endothelial barrier disruption by cleaving key junctional protein VE-cadherin
AU - Tseng, Esther
AU - Yee Teoh, Sonia Soo
AU - Wang, Yao
AU - Nie, Guiying
PY - 2019/1/1
Y1 - 2019/1/1
N2 - 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.
AB - 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.
KW - Endothelial barrier
KW - HtrA4
KW - Oedema
KW - Preeclampsia
KW - Vascular permeability
KW - VE-Cadherin
UR - http://www.scopus.com/inward/record.url?scp=85059677664&partnerID=8YFLogxK
U2 - 10.1016/j.placenta.2019.01.001
DO - 10.1016/j.placenta.2019.01.001
M3 - Article
JO - Placenta
JF - Placenta
SN - 0143-4004
ER -