Maternal serum soluble fms-like tyrosine kinase 1 concentrations are not increased in early pregnancy and decrease more slowly postpartum in women who develop preeclampsia

Powers, Robert W.; Roberts, James M.; Cooper, Katheryn M.; Gallaher, Marcia J.; Frank, Michael P.; Harger, Gail; Ness, Roberta B.

doi:10.1016/j.ajog.2004.11.038

Cited by 120 publications

(91 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although numerous studies have implicated sFLT1 in the pathogenesis of hypertension in preeclampsia, the underlying molecular mechanism is not fully understood. Consistent with previous studies in both mouse models and preeclamptic women, the onset of hypertension in the Endo-VEGF animals in our study occurred well before term, when sFLT1 levels, although elevated, are similar to or even lower than the control levels at term (40,41), yet control animals do not develop hypertension. It is likely that the sensitivity of hypertension to sFLT1 levels varies throughout pregnancy (30) and that the threshold level for development of hypertension at early stages is lower than it is at later stages.…”

Section: Discussionsupporting

confidence: 92%

Endometrial VEGF induces placental sFLT1 and leads to pregnancy complications

Fan¹,

Rai²,

Kambham³

et al. 2014

J. Clin. Invest.

163

166

View full text Add to dashboard Cite

Figure 8. Effects of placental sFlt1 knockdown with or without endometrial VEGF overexpression. (A-L) Placental sFlt1 knockdown. Upon placentaspecific sFLT1 shRNA expression, widespread hemorrhaging in the fetus (B) and at the placental-decidual junction (D) was observed on GD18 compared with controls (A and C). Histological examination of sFLT1 shRNA-expressing placentas revealed extraordinary dilation of some maternal blood sinuses (arrowheads) in the labyrinth (E and F) and fibrin deposition (arrow) in these spaces (G and H). (I and J) MSB staining revealed extravasated fibrin (arrow) in adjacent areas. Placental sFlt1 knockdown did not affect implantation rate (K), whereas the fetal resorption rate significantly increased (L). (M-V) Placental sFlt1 knockdown enhanced the deleterious effects in Endo-VEGF animals. Pregnancies surviving to GD16 exhibited (M) excessive vaginal bleeding and (N-P) termination of pregnancy or resorption (arrows denote resorption sites) as well as (Q) widespread and extensive hemorrhaging in fetuses and placentas (arrowheads) and in deciduas at the maternal-fetal junction (asterisk). Histological examination (R-T) revealed widespread dilation and congestion of maternal blood sinuses (arrowheads) in the labyrinth, venous sinuses, and veins at maternal-fetal junctions, and MSB staining (U and V) demonstrated extensive fibrin extravasation (arrows) in the labyrinth and at the maternal-fetal junction. Results are mean ± SD. *P < 0.05 (n = 15). Scale bars: 2 mm (A-D); 500 μm (E, F, and R); 50 μm (G-J); 100 μm (S-V).

show abstract

Section: Discussionsupporting

confidence: 92%

Endometrial VEGF induces placental sFLT1 and leads to pregnancy complications

Fan¹,

Rai²,

Kambham³

et al. 2014

J. Clin. Invest.

163

166

View full text Add to dashboard Cite

show abstract

“…A number of candidates have been proposed, especially pro-angiogenic and anti-angiogenic factors, and while they have repeatedly demonstrated changes in many women with established disease, they have shown poor sensitivity and specifi city in predicting all forms of preeclampsia (11)(12)(13). Therefore, there continues to be a need for predictive biomarkers of this disorder with more reliable sensitivities and specifi cities.…”

Section: Discussionmentioning

confidence: 99%

“…Collectively, these data suggest that there are biochemical abnormalities that occur prior to clinically evident preeclampsia signs and symptoms. However, to date, there are still no accepted predictive biomarkers for this disease (11)(12)(13) despite some initial promise for a number of proposed candidates. Also, currently, the specifi c causes (as opposed to consequences) of preeclampsia are still debated and have yet to be established.…”

Section: Mass Spectrometric Analysis Of the Lipid Extractmentioning

confidence: 99%

Detection and confirmation of serum lipid biomarkers for preeclampsia using direct infusion mass spectrometry

Anand

Young

Esplin

et al. 2016

Journal of Lipid Research

View full text Add to dashboard Cite

“…These include multi-gestational pregnancies, high altitude pregnancies, trisomy 13, and nulliparity (Bdolah et al, 2006a,b;Nevo et al, 2006;Wolf et al, 2005). Furthermore a decrease in circulating sFlt1 levels amongst smokers may explain the decreased incidence of preeclampsia in this subgroup (Levine et al, 2006;Powers et al, 2005).…”

Section: Angiogenic Factors In the Pathogenesis Of Preeclampsiamentioning

confidence: 99%

Angiogenic factors and natural killer (NK) cells in the pathogenesis of preeclampsia

Kopcow

Karumanchi

2007

Journal of Reproductive Immunology

View full text Add to dashboard Cite

Preeclampsia is a pregnancy-specific complex disease in which numerous genetic, immunological and environmental factors interact. Characterized by new onset hypertension, proteinuria and edema after 20 weeks of gestation, preeclampsia is often complicated by small-for-gestational-age (SGA) babies and preterm delivery, and is therefore a significant cause of maternal and fetal morbidity and mortality. The only definitive treatment of preeclampsia is delivery of the placenta. Recent data suggest that the anti-angiogenic state induced by excess circulating anti-angiogenic factors of placental origin may be responsible for the clinical signs and symptoms of preeclampsia. Natural killer (NK) cells at the maternal/fetal interface, which are thought to play an important role in normal placental development, have been noted recently to induce angiogenic factors and vascular remodeling. Moreover, genetic studies suggest that susceptibility to preeclampsia may be influenced by polymorphic HLA-C ligands and killer cell receptors (KIR) present on NK cells. This review summarizes our current understanding of the role of angiogenic factors and NK cells in the pathogenesis of preeclampsia.

show abstract

Maternal serum soluble fms-like tyrosine kinase 1 concentrations are not increased in early pregnancy and decrease more slowly postpartum in women who develop preeclampsia

Cited by 120 publications

References 24 publications

Endometrial VEGF induces placental sFLT1 and leads to pregnancy complications

Endometrial VEGF induces placental sFLT1 and leads to pregnancy complications

Detection and confirmation of serum lipid biomarkers for preeclampsia using direct infusion mass spectrometry

Angiogenic factors and natural killer (NK) cells in the pathogenesis of preeclampsia

Contact Info

Product

Resources

About