Elevated plasma endothelial microparticles in preeclampsia (original) (raw)
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Elevated plasma endothelial microparticles: Preeclampsia versus gestational hypertension
American Journal of Obstetrics and Gynecology, 2004
Objective: Elevated plasma endothelial microparticle levels have been found to be elevated in women with preeclampsia. However, their role in distinguishing preeclampsia from gestational hypertension remains to be elucidated. The objectives of this study were to compare endothelial microparticle levels among patients with preeclampsia, gestational hypertension, and healthy pregnant control subjects and to evaluate the effect of plasma from women with preeclampsia and gestational hypertension on the release of endothelial microparticles by renal microvascular endothelial cells.
Endothelial microparticles and the antiangiogenic state in preeclampsia and the postpartum period
American Journal of Obstetrics and Gynecology, 2012
OBJECTIVE(S)-To determine if endothelial microparticles (EMPs), markers of endothelial damage, are associated with soluble fms-like tyrosine kinase 1 (sFlt1), soluble endoglin (sEnd), and placental growth factor (PlGF) in women with preeclampsia. STUDY DESIGN: A prospective cohort study was conducted on 20 preeclamptic women and 20 controls. EMP's measured by flow cytometry, sFlt1, sEnd, and PlGF were measured at time of enrollment, 48 hours, and 1 week postpartum. RESULTS-Preeclamptic CD31+/42−, CD 62E+, and CD105+ EMP levels were significantly elevated in preeclamptics vs. controls at time of enrollment. The sFlt1:PlGF ratio was correlated with CD31+/42− and CD 105+ EMPs (r=0.69 and r=0.51, respectively) in preeclampsia. Levels of CD31+/42− EMPs remained elevated 1-week postpartum (p=0.026). CONCLUSIONS-EMPs are elevated in preeclampsia. The correlation of EMPs and the sFlt1:PlGF ratio suggests that anti-angiogenesis is related to apoptosis of the endothelia. Endothelial damage persists one week after delivery.
Markers of Endothelial Injury and Dysfunction in Early- and Late-Onset Preeclampsia
Life, 2020
With regard to differences in the clinical symptoms of preeclampsia (PE), the degree of endothelial dysfunction may differ between early and late-onset preeclampsia (EOP and LOP). The authors of this study examined it by assessing the endothelial injury level in women with EOP (20 patients) and LOP (20 patients) and in normotensive pregnant women (20 patients) in their late second and third trimesters of pregnancy, using the two markers—the serum concentration of hyaluronan (HA) and the serum level of soluble vascular cell adhesion molecule-1 (sVCAM-1). The serum concentrations of HA and sVCAM-1 did not differ significantly between the EOP and LOP patients. However, these were statistically higher than that of the control group participants (p < 0.05; p < 0.001). A significant correlation between the levels of HA and sVCAM-1 was found both in the entire group of patients with preeclampsia (p = 0.0277) and in women with late-onset disease (p = 0.0364), but not in the patients w...
Endothelial dysfunction in the pathogenesis of pre-eclampsia
Frontiers in Bioscience, 2014
Introduction 3. Pathogenesis 3.1. Abnormal development of the placenta 3.2. Remodeling of the spiral arteries 3.3. Hypoperfusion, hypoxia, and ischemia of the placenta 3.4. Systemic endothelial dysfunction 3.4.1. Imbalance between angiogenic and anti-angiogenic factors 3.4.1.1. VEGF and PlGF 3.4.1.2. SEng 3.4.2. The role of circulating endothelial cells (CECs), endothelial progenitor cells (EPCs), and microparticles in pre-eclampsia 3.
The endothelial-platelet dysfunction in preeclampsia
Preeclampsia is a common, pregnancy-specific syndrome defined by clinical findings of elevated blood pressure combined with proteinuria and edema. It is characterized by a generalized dysfunction of the maternal endothelium, as demonstrated by the increased levels of factor VIII, total and cellular fibronectin, thrombomodulin, endothelin and a disturbance of prostacyclin/thromboxane balance. The new concept of endothelial-platelet dysfunction shows the central role of endothelial cell and platelet: endothelial dysfunction, increased vascular reactivity and platelet activation. The aim of this review is to reveal the recent data regarding the role of endothelial-platelet dysfunction in the pathogenesis of preeclampsia.
Hypertension, 2005
The pathophysiology of preeclampsia involves the release of a circulating factor(s) from a hypoperfused placenta that activates the maternal endothelium. This study investigated the effect on in vitro endothelial function of plasma taken from women in whom preeclampsia subsequently developed. Women at increased risk for an adverse pregnancy outcome were identified using Doppler waveform analysis. Plasma samples (22 and 26 weeks) were incubated with myometrial vessels taken from women with uncomplicated pregnancies. Wire myography was used to study the effect of plasma on the endothelium-dependent vessel behavior. Incubation of vessels from normal pregnant women with plasma from women in whom preeclampsia subsequently developed (nϭ19) significantly reduced endothelium-dependent relaxation, compared with vessels incubated with plasma from normal pregnant women (nϭ48). This effect was demonstrable for plasma taken at 22 weeks (residual constriction 47.1Ϯ6.6% versus 32.0Ϯ4.4%, Pϭ0.004 at 1-hour incubation; and 59.1Ϯ8.4% versus 42.3Ϯ5.9%, Pϭ0.001 at 18-hour incubation) and 26 weeks (59.2Ϯ5.2% versus 29.1Ϯ5.6%, PϽ0.001 at 1 hour; and 63.3Ϯ7.6% versus 31.9 ϩ/-7.2%, PϽ0.0001 at 18 hours). Endothelial-dependent relaxation was unaltered after incubation with plasma taken from women in whom normotensive intrauterine growth restriction subsequently developed (nϭ19). This study supports the hypothesis that plasma, from women in whom preeclampsia develops, collected weeks before diagnosis is capable of altering endothelial function. (Hypertension. 2005;45:1-6.)
Emerging Role of Endothelial and Inflammatory Markers in Preeclampsia
Disease Markers, 2009
Objectives: Endothelial disturbance and excess inflammatory response are pathogenic mechanisms in pre-eclampsia (PE). Authors determine the clinical diagnostic role for thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1) as endothelial markers and C-reactive protein (CRP), and interlukin-6 (IL-6) as inflammatory markers when tested independently or in combinations.
Endothelial barrier function in preeclampsia
Frontiers in Bioscience, 2007
Introduction 3. Increased vascular permeability in preeclampsia 3.1. Endothelial function during pregnancy 3.2. Imbalance of plasma and interstitial colloid osmotic pressure and capillary hydrostatic pressure in preeclampsia 3.3. Evidence of increased vascular permeability during preeclampsia 4. HUVECs as a model to study endothelial barrier function in vitro 4.1. Electron microscopic findings 4.2. Altered endothelial junctional protein distribution and expression for VE-cadherin and occludin, key cell structure basis of disturbed endothelial barrier function in preeclampsia 5. Endothelial components involved in regulation of endothelial barrier function in preeclampsia 5.1. Caveolae and endothelial NO synthase (eNOS) 5.2. Focal adhesion kinase 5.3. Adenosine triphosphate (ATP) 5.4. Glycocalyx 6. Circulating mediators that may disrupt endothelial barrier function in preeclampsia 6