Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.

Pre-eclampsia is a complication of pregnancy associated with activation of coagulation. It is caused by the placenta, which sheds increased amounts of syncytiotrophoblast microvesicles (STBM) into the maternal circulation. We hypothesized that STBM could contribute to the haemostatic activation obse...

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Main Authors: Chris Gardiner, Dionne S Tannetta, Carol A Simms, Paul Harrison, Christopher W G Redman, Ian L Sargent
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3194796?pdf=render
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spelling doaj-9c116e99c0aa425a8860e04746ef6a0a2020-11-24T22:04:57ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-01610e2631310.1371/journal.pone.0026313Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.Chris GardinerDionne S TannettaCarol A SimmsPaul HarrisonChristopher W G RedmanIan L SargentPre-eclampsia is a complication of pregnancy associated with activation of coagulation. It is caused by the placenta, which sheds increased amounts of syncytiotrophoblast microvesicles (STBM) into the maternal circulation. We hypothesized that STBM could contribute to the haemostatic activation observed in pre-eclampsia.STBM were collected by perfusion of the maternal side of placentae from healthy pregnant women and women with pre-eclampsia at caesarean section. Calibrated automated thrombography was used to assess thrombin generation triggered by STBM-borne tissue factor in platelet poor plasma (PPP). No thrombin was detected in PPP alone but the addition of STBM initiated thrombin generation in 14/16 cases. Pre-eclampsia STBM significantly shortened the lag time (LagT, P = 0.01) and time to peak thrombin generation (TTP, P = 0.005) when compared to normal STBM. Blockade of tissue factor eliminated thrombin generation, while inhibition of tissue factor pathway inhibitor significantly shortened LagT (p = 0.01) and TTP (P<0.0001), with a concomitant increase in endogenous thrombin potential.STBM triggered thrombin generation in normal plasma in a tissue factor dependent manner, indicating that TF activity is expressed by STBM. This is more pronounced in STBM shed from pre-eclampsia placentae. As more STBM are shed in pre-eclampsia these observations give insight into the disordered haemostasis observed in this condition.http://europepmc.org/articles/PMC3194796?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Chris Gardiner
Dionne S Tannetta
Carol A Simms
Paul Harrison
Christopher W G Redman
Ian L Sargent
spellingShingle Chris Gardiner
Dionne S Tannetta
Carol A Simms
Paul Harrison
Christopher W G Redman
Ian L Sargent
Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
PLoS ONE
author_facet Chris Gardiner
Dionne S Tannetta
Carol A Simms
Paul Harrison
Christopher W G Redman
Ian L Sargent
author_sort Chris Gardiner
title Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
title_short Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
title_full Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
title_fullStr Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
title_full_unstemmed Syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
title_sort syncytiotrophoblast microvesicles released from pre-eclampsia placentae exhibit increased tissue factor activity.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2011-01-01
description Pre-eclampsia is a complication of pregnancy associated with activation of coagulation. It is caused by the placenta, which sheds increased amounts of syncytiotrophoblast microvesicles (STBM) into the maternal circulation. We hypothesized that STBM could contribute to the haemostatic activation observed in pre-eclampsia.STBM were collected by perfusion of the maternal side of placentae from healthy pregnant women and women with pre-eclampsia at caesarean section. Calibrated automated thrombography was used to assess thrombin generation triggered by STBM-borne tissue factor in platelet poor plasma (PPP). No thrombin was detected in PPP alone but the addition of STBM initiated thrombin generation in 14/16 cases. Pre-eclampsia STBM significantly shortened the lag time (LagT, P = 0.01) and time to peak thrombin generation (TTP, P = 0.005) when compared to normal STBM. Blockade of tissue factor eliminated thrombin generation, while inhibition of tissue factor pathway inhibitor significantly shortened LagT (p = 0.01) and TTP (P<0.0001), with a concomitant increase in endogenous thrombin potential.STBM triggered thrombin generation in normal plasma in a tissue factor dependent manner, indicating that TF activity is expressed by STBM. This is more pronounced in STBM shed from pre-eclampsia placentae. As more STBM are shed in pre-eclampsia these observations give insight into the disordered haemostasis observed in this condition.
url http://europepmc.org/articles/PMC3194796?pdf=render
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