Reduction of serum-induced endothelial STAT3(Y705) activation is associated with preeclampsia

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Reduction of serum-induced endothelial STAT3(Y705) activation is associated with preeclampsia. / Christensen, M.; Petersen, J. L.; Sivanandam, P. et al.

I: Pregnancy Hypertension, Bind 25, 08.2021, s. 103-109.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

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Christensen, M. ; Petersen, J. L. ; Sivanandam, P. et al. / Reduction of serum-induced endothelial STAT3(Y705) activation is associated with preeclampsia. I: Pregnancy Hypertension. 2021 ; Bind 25. s. 103-109.

Bibtex

@article{d693291b425643599b690882b801df12,
title = "Reduction of serum-induced endothelial STAT3(Y705) activation is associated with preeclampsia",
abstract = "Objectives: Preeclampsia is associated with maternal morbidity and mortality during pregnancy, and also an increased cardiovascular disease (CVD) risk later in life. During preeclampsia, alterations in secreted placental factors leading to systemic maternal endothelial dysfunction are evident. However, little is known about the associated endothelial intracellular signaling. STAT3 is a latent cytoplasmic transcription factor involved in endothelial cell differentiation, survival, and angiogenesis. We aimed to test if preeclampsia and preeclampsia-related placental factors could alter serum-induced STAT3(Y705) activation in endothelial cells. Furthermore, if altered serum-induced endothelial STAT3 (Y705) activation is related to post-preeclamptic CVD risk. Study design: HUVECs were used as a model of maternal endothelium. Experiments entailed addition of 20% human pregnancy serum as well as addition of recombinant PlGF, sFLT1 and VEGF-A165a to the cells. Main outcome measures: Levels of pSTAT3(Y705) related to STAT3 levels were evaluated by immunoblotting analysis. Results: Our results show that preeclamptic serum induces significantly lower STAT3(Y705) phosphorylation compared with uncomplicated pregnancy serum (P = 0.0089) in endothelial cells. Furthermore, STAT3(Y705) phosphorylation was not changed upon addition of PlGF, sFLT1, or VEGF-A165a together with pregnancy sera compared with sera alone. Finally, sera from women with previous preeclampsia and current hypertension and carotid atherosclerotic plaques show significantly lower STAT3(Y705) phosphorylation capabilities compared with healthy women with previous uncomplicated pregnancies 8–18 years after deliveries (P = 0.029). Conclusions: Reduction in serum-induced endothelial STAT3(Y705) activation may play an important role in the preeclampsia-associated endothelial dysfunction. Additionally, reduced endothelial STAT3(Y705) phosphorylation may contribute to increased post-preeclamptic CVD risk 8–18 years after delivery.",
keywords = "Cardiovascular disease, HUVECs, Preeclampsia, STAT3, VEGF",
author = "M. Christensen and Petersen, {J. L.} and P. Sivanandam and Kronborg, {C. S.} and Knudsen, {U. B.} and Martensen, {P. M.}",
note = "Publisher Copyright: {\textcopyright} 2021 International Society for the Study of Hypertension in Pregnancy",
year = "2021",
month = aug,
doi = "10.1016/j.preghy.2021.05.012",
language = "English",
volume = "25",
pages = "103--109",
journal = "Pregnancy Hypertension",
issn = "2210-7789",
publisher = "Elsevier BV",

}

RIS

TY - JOUR

T1 - Reduction of serum-induced endothelial STAT3(Y705) activation is associated with preeclampsia

AU - Christensen, M.

AU - Petersen, J. L.

AU - Sivanandam, P.

AU - Kronborg, C. S.

AU - Knudsen, U. B.

AU - Martensen, P. M.

N1 - Publisher Copyright: © 2021 International Society for the Study of Hypertension in Pregnancy

PY - 2021/8

Y1 - 2021/8

N2 - Objectives: Preeclampsia is associated with maternal morbidity and mortality during pregnancy, and also an increased cardiovascular disease (CVD) risk later in life. During preeclampsia, alterations in secreted placental factors leading to systemic maternal endothelial dysfunction are evident. However, little is known about the associated endothelial intracellular signaling. STAT3 is a latent cytoplasmic transcription factor involved in endothelial cell differentiation, survival, and angiogenesis. We aimed to test if preeclampsia and preeclampsia-related placental factors could alter serum-induced STAT3(Y705) activation in endothelial cells. Furthermore, if altered serum-induced endothelial STAT3 (Y705) activation is related to post-preeclamptic CVD risk. Study design: HUVECs were used as a model of maternal endothelium. Experiments entailed addition of 20% human pregnancy serum as well as addition of recombinant PlGF, sFLT1 and VEGF-A165a to the cells. Main outcome measures: Levels of pSTAT3(Y705) related to STAT3 levels were evaluated by immunoblotting analysis. Results: Our results show that preeclamptic serum induces significantly lower STAT3(Y705) phosphorylation compared with uncomplicated pregnancy serum (P = 0.0089) in endothelial cells. Furthermore, STAT3(Y705) phosphorylation was not changed upon addition of PlGF, sFLT1, or VEGF-A165a together with pregnancy sera compared with sera alone. Finally, sera from women with previous preeclampsia and current hypertension and carotid atherosclerotic plaques show significantly lower STAT3(Y705) phosphorylation capabilities compared with healthy women with previous uncomplicated pregnancies 8–18 years after deliveries (P = 0.029). Conclusions: Reduction in serum-induced endothelial STAT3(Y705) activation may play an important role in the preeclampsia-associated endothelial dysfunction. Additionally, reduced endothelial STAT3(Y705) phosphorylation may contribute to increased post-preeclamptic CVD risk 8–18 years after delivery.

AB - Objectives: Preeclampsia is associated with maternal morbidity and mortality during pregnancy, and also an increased cardiovascular disease (CVD) risk later in life. During preeclampsia, alterations in secreted placental factors leading to systemic maternal endothelial dysfunction are evident. However, little is known about the associated endothelial intracellular signaling. STAT3 is a latent cytoplasmic transcription factor involved in endothelial cell differentiation, survival, and angiogenesis. We aimed to test if preeclampsia and preeclampsia-related placental factors could alter serum-induced STAT3(Y705) activation in endothelial cells. Furthermore, if altered serum-induced endothelial STAT3 (Y705) activation is related to post-preeclamptic CVD risk. Study design: HUVECs were used as a model of maternal endothelium. Experiments entailed addition of 20% human pregnancy serum as well as addition of recombinant PlGF, sFLT1 and VEGF-A165a to the cells. Main outcome measures: Levels of pSTAT3(Y705) related to STAT3 levels were evaluated by immunoblotting analysis. Results: Our results show that preeclamptic serum induces significantly lower STAT3(Y705) phosphorylation compared with uncomplicated pregnancy serum (P = 0.0089) in endothelial cells. Furthermore, STAT3(Y705) phosphorylation was not changed upon addition of PlGF, sFLT1, or VEGF-A165a together with pregnancy sera compared with sera alone. Finally, sera from women with previous preeclampsia and current hypertension and carotid atherosclerotic plaques show significantly lower STAT3(Y705) phosphorylation capabilities compared with healthy women with previous uncomplicated pregnancies 8–18 years after deliveries (P = 0.029). Conclusions: Reduction in serum-induced endothelial STAT3(Y705) activation may play an important role in the preeclampsia-associated endothelial dysfunction. Additionally, reduced endothelial STAT3(Y705) phosphorylation may contribute to increased post-preeclamptic CVD risk 8–18 years after delivery.

KW - Cardiovascular disease

KW - HUVECs

KW - Preeclampsia

KW - STAT3

KW - VEGF

UR - http://www.scopus.com/inward/record.url?scp=85107755672&partnerID=8YFLogxK

U2 - 10.1016/j.preghy.2021.05.012

DO - 10.1016/j.preghy.2021.05.012

M3 - Journal article

C2 - 34098522

AN - SCOPUS:85107755672

VL - 25

SP - 103

EP - 109

JO - Pregnancy Hypertension

JF - Pregnancy Hypertension

SN - 2210-7789

ER -