Placental hypoxia-induced alterations in vascular function, morphology, and endothelial barrier integrity

  title={Placental hypoxia-induced alterations in vascular function, morphology, and endothelial barrier integrity},
  author={Philippe Vangrieken and Alex H. V. Remels and Salwan Al-Nasiry and Aalt Bast and Ger M. J. Janssen and Ulrike von Rango and Daan Vroomans and Yannick C. W. Pinckers and Frederik Jan van Schooten and Paul M H Schiffers},
  journal={Hypertension Research},
Preeclampsia (PE) is a pregnancy-related disorder characterized by hypertension and proteinuria that affects 3–10% of all pregnancies. Although its pathophysiology remains obscure, placental hypoxia-induced oxidative stress and alterations in vascular function, morphology, and endothelial barrier integrity are considered to play a key role in the development of preeclampsia. In this study, placental villous explants of noncomplicated placentae and BeWo cells were subjected to hypoxia. The… 
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Hypoxia-induced mitochondrial abnormalities in cells of the placenta.
This study is the first to demonstrate that placental hypoxia is associated with mitochondrial-generated reactive oxygen species and significant alterations in the molecular pathways controlling mitochondrial content and function and indicates that targeting mitochondrial oxidative stress may have therapeutic benefit in the management of pathologies related to placental Hypoxia.
Protective Effect of Artemisinin on the Placenta of L-NAME Induced rat model of Preeclampsia
It is concluded that ART exerted protective effect in preeclampsia model through oxidative stress correction and reduction of proteinuria along with improvement of placental vascular and cellular changes in both light and electron microscopies.
Melatonin ameliorates hypertension in hypertensive pregnant mice and suppresses the hypertension-induced decrease in Ca2+-activated K+ channels in uterine arteries
Melatonin ameliorates hypertension in hypertensive pregnant mice and suppresses hypertension-induced decreases in Ca2+-activated K+ channels in uterine arteries.
Application Research Progress of Ultrasonic Evaluation of Placental Function
Great importance to understand the structure and function of the placenta, early placental function assessment, application of two-dimensional ultrasound imaging and colorDoppler ultrasound blood flow imaging, 3 d power doppler imaging, ultrasound elastography mode ultrasonic imaging method, multimodal way of ultra-* sonic imaging evaluation placentalfunction to improve the outcome and improve the obstetric quality have the very vital significance.
Melatonin and gestational hypertension
New findings indicate that melatonin is a key player with direct health benefits rather than a secondary player acting only through sleep, as well as antihypertension, anticancer, antiapoptotic, and antiplatelet effects.


The direct and sustained consequences of severe placental hypoxia on vascular contractility
An in vitro model of preeclampsia was developed which found that agonists for the angiotensin-I and endothelin-1 receptor released by placental tissue under severe hypoxia provoke vasoconstriction, and the dietary antioxidant quercetin could partially prevent the acute and sustained vascular effects in a concentration-dependent manner.
Placental trophoblast-derived factors diminish endothelial barrier function.
It is concluded that placental trophoblast cells produce factors that diminish the barrier function of endothelial cells and endothelial tight junctions are more susceptible to factors released from preeclamptic trophoplast cells than from normal trophOBlast cells, which implicate troPHoblast-derived factors in the increased vascular permeability associated with preeclampsia.
Endothelin-1 triggers placental oxidative stress pathways: putative role in preeclampsia.
It is postulated that ET-1 may be one of the key links between primary placental disorders and the systemic endothelial dysfunction of PE by altering the balance between oxidant and antioxidant forces in favor of oxidation.
Association of maternal endothelial dysfunction with preeclampsia.
The results indicate that endothelial function is impaired in women with previous preeclampsia and is not explained by established maternal risk factors but is reversed by antioxidant ascorbic acid administration.
Endothelin: key mediator of hypertension in preeclampsia.
Antagonism of the endothelin-A receptor has proved beneficial in numerous animal models of gestational hypertension, and it remains an intriguing target for pharmacological intervention in preeclampsia.
Hypertension Produced by Reduced Uterine Perfusion in Pregnant Rats Is Associated With Increased Soluble Fms-Like Tyrosine Kinase-1 Expression
The hypothesis that RUPP increases the expression of sFlt-1 and alters the balance of angiogenic factors in the maternal circulation is supported and the RUPp model of pregnancy-induced hypertension may provide an invaluable model for mechanistic studies into the role of s Flt- 1 in the pathogenesis of preeclampsia.
Decreased endothelium-dependent vascular relaxation during reduction of uterine perfusion pressure in pregnant rat.
An endothelium-dependent relaxation pathway involving the release of NO from endothelial cells and increased cGMP production in smooth muscle is inhibited in systemic vessels of late pregnant rats with reduced uterine perfusion pressure and may in part explain the increased vascular resistance in pregnancy-induced hypertension.