Increased expression of sFlt-1 in in vivo and in vitro models of human placental hypoxia is mediated by HIF-1 (Q57105968)

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19 January 2020

title

Increased expression of sFlt-1 in in vivo and in vitro models of human placental hypoxia is mediated by HIF-1 (English)

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Stacy Zamudio

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1

Ori Nevo

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19 January 2020

author name string

Nima Soleymanlou

2

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Yuan Wu

3

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Jing Xu

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John Kingdom

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Ariel Many

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language of work or name

English

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publication date

20 April 2006

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American Journal of Physiology - Regulatory, Integrative and Comparative Physiology

19 January 2020

published in

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volume

291

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19 January 2020

page(s)

R1085-93

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issue

4

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ACOG technology assessment. Genetics and molecular diagnostic testing. Number 1, July 2002. American College of Obstetrics and Gynecology

19 January 2020

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Differential transcriptional regulation of the two vascular endothelial growth factor receptor genes. Flt-1, but not Flk-1/KDR, is up-regulated by hypoxia.

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In vitro ischemia-reperfusion injury in term human placenta as a model for oxidative stress in pathological pregnancies

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Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation

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Inhibition of vascular endothelial cell growth factor activity by an endogenously encoded soluble receptor

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Elevated Serum Soluble Vascular Endothelial Growth Factor Receptor 1 (sVEGFR-1) Levels in Women with Preeclampsia

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Hypoxia-induced increase in soluble Flt-1 production correlates with enhanced oxidative stress in trophoblast cells from the human placenta.

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Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

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Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

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Cytotrophoblasts up-regulate soluble fms-like tyrosine kinase-1 expression under reduced oxygen: an implication for the placental vascular development and the pathophysiology of preeclampsia

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Altered blood pressure course during normal pregnancy and increased preeclampsia at high altitude (3100 meters) in Colorado

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Evidence for the functional activity of hypoxia-inducible transcription factors overexpressed in preeclamptic placentae

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Trophoblast deportation and the maternal inflammatory response in pre-eclampsia

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Oxidative stress due to hypoxia/reoxygenation induces angiogenic factor VEGF in adult rat myocardium: possible role of NFkappaB.

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A novel Mtd splice isoform is responsible for trophoblast cell death in pre-eclampsia

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Oxygen and placental vascular development

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Hypoxia activates the human placental vascular endothelial growth factor system in vitro and in vivo: up-regulation of vascular endothelial growth factor in clinically relevant hypoxic ischemia in birth asphyxia

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Flt-1 but not KDR/Flk-1 tyrosine kinase is a receptor for placenta growth factor, which is related to vascular endothelial growth factor.

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A Vascular Endothelial Growth Factor Antagonist Is Produced by the Human Placenta and Released into the Maternal Circulation1

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DOI

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19 January 2020

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