Flow Cytometric Detection of Activated Platelets in Pregnant Women Prior to the Development of Pre-Eclampsia

Janes, Sarah L.; Kyle, Phillipa M.; Redman, Christopher W.G.; Goodall, Alison H.

doi:10.1055/s-0038-1649882

Cited by 103 publications

(73 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As a result, the phenotype of decidual leukocytes might be different in preeclampsia, a possibility we are currently examining. Preeclamptic cytotrophoblasts also fail to express PECAM-1, raising the additional possibility that they have faulty interactions with platelets, a particularly intriguing possibility because platelet activation is a frequent complication of preeclampsia (35).…”

Section: Discussionmentioning

confidence: 99%

Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome?

Zhou

Damsky²,

Fisher³

1997

J. Clin. Invest.

857

480

View full text Add to dashboard Cite

In human pregnancy, placental cytotrophoblasts that invade the uterus downregulate the expression of adhesion receptors that are characteristic of their epithelial origin, and upregulate the expression of adhesion receptors that are expressed by vascular cells. We suggest that this transformation could be critical to endovascular invasion, the process whereby cytotrophoblasts invade the uterine spiral arterioles and line their walls (Zhou et al. J. Clin. Invest. 1997. 99: 2139-2151.). To better understand the in vivo significance of these findings, we tested the hypothesis that in preeclampsia, an important disease of pregnancy in which endovascular invasion is abrogated, cytotrophoblasts fail to adopt a vascular adhesion phenotype. In experiments described here we stained placental bed biopsy specimens from age-matched control pregnancies and from those complicated by preeclampsia with antibodies that recognize adhesion molecules that are normally modulated during this transformation. In preeclampsia, differentiating/invading cytotrophoblasts fail to express properly many of these molecules, including integrin, cadherin, and Ig superfamily members. These results suggest that preeclampsia is associated with failure of cytotrophoblasts to mimic a vascular adhesion phenotype. The functional consequences of this abnormality are unknown, but are likely to affect negatively cytotrophoblast endovascular invasion and uterine arteriole remodeling, thereby compromising blood flow to the maternal-fetal interface. ( J. Clin. Invest. 1997. 99:2152-2164.)

show abstract

Section: Discussionmentioning

confidence: 99%

Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome?

Zhou

Damsky²,

Fisher³

1997

J. Clin. Invest.

857

480

View full text Add to dashboard Cite

show abstract

“…Activation of the coagulation cascade, especially alterations in platelet function, can be demonstrated weeks to months before clinically evident disease. 54,55 Similarly, increased sensitivity to angiotensin 46 and reduced plasma volume 56 have been found in groups of women destined to develop PE. It is important to point out that these changes are not universally present and thus can only be recognised in groups of women destined to develop PE.…”

Section: Endothelial Dysfunction In Pre-eclampsiamentioning

confidence: 93%

Hypertension in pregnancy

Pipkin

Roberts

2000

J Hum Hypertens

View full text Add to dashboard Cite

Hypertension arising during pregnancy remains one of the two most frequently-cited causes of maternal death in the UK. In some cases, pregnancy is unmasking underlying hypertension, which manifests itself in later life. Pregnant women who develop de novo proteinuric hypertension (pre-eclampsia, PE) can share many risk factors with patients with the metabolic syndrome, such as obesity, dyslipidaemia and insulin resistance. However, more than half the women who develop PE remain normotensive thereafter. There is a genetic component(s) to the disease, but it is most improbable that there is a 'PE gene'. Rather, there are factors such as geneticallydetermined thrombophilias which are predisposers but not prerequisites. Impaired placentation is a feature, with inadequate invasion of the spiral arteries by syncytiotrophoblast and poor remodelling. However, similiar features are found in association with non-hypertensive

show abstract

“…4' 5 An example of flow cytometric detection of platelet activation in preeclarnpsia is the finding by Janes and Goodall 6 of a significantly increased platelet surface expression of CD63, a marker for secretion of platelet lysosomal granules, compared with normotensive pregnancy. In a prospective study Janes et al 7 also found an increased expression of CD63 at 28 weeks' gestation in pregnant women before the development of preeclarnpsia.…”

mentioning

confidence: 87%

Extensive platelet activation in preeclampsia compared with normal pregnancy: Enhanced expression of cell adhesion molecules

Konijnenberg¹,

Stokkers²,

Post³

et al. 1997

American Journal of Obstetrics and Gynecology

138

View full text Add to dashboard Cite

Extensive platelet activation in preeclampsia compared with normal pregnancy: enhanced expression of cell adhesion molecules Konijnenberg, A.; Stokkers, E.W.; van der Post, J.A.M.; Schaap, M.C.L.; Boer, K.; Bleker, O.P.; Sturk, A. Published in:American journal of obstetrics and gynecology DOI:10.1016/S0002-9378(97) Link to publication Citation for published version (APA): Konijnenberg, A., Stokkers, E. W., van der Post, J. A. M., Schaap, M. C. L., Boer, K., Bleker, O. P., & Sturk, A. (1997). Extensive platelet activation in preeclampsia compared with normal pregnancy: enhanced expression of cell adhesion molecules. American journal of obstetrics and gynecology, 176, 461-469. https://doi.org/10.1016/S0002-9378(97)70516-7 General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Amsterdam and Leiden, The Netherlands OBJECTIVES= Platelets play an important role in the pathophysiologic mechanisms of preeclampsia. Our purpose was to investigate by means of flow cytometry to what extent platelets circulate in an activated state during normal pregnancy and whether this activation is more extensive in preeclampsia. STUDY DESIGN= Platelets in whole blood from 10 preeclamptic third-trimester pregnant women (highest diastolic blood pressure range 100 to 130 mm Hg, proteinuria range 0.59 to 11.5 gm/24 hr) and from 10 normotensive third-trimester pregnant controls were analyzed with the following activation markers: anti-P-selectin (a-granule secretion), anti-CD63 (lysosomal secretion), PAC-1 (monoclonal antibody against fibrinogen receptor conformation of the glycoprotein lib/Ilia complex), anti-platelet endothelial cell adhesion molecule-I, and annexin-V (a placental protein that binds to negatively charged phospholipids, present on the outside of the platelet plasma membrane after activation). The differences in surface antigen exposure between the two groups were determined by double-label flow cytometry. Flow cytometric data were analyzed in two ways: first, the percentages of activated platelets above a certain threshold compared with a nonpregnant control sample were determined, indicative for activation of a subpopulation of cells, and, second, the mean fluorescence intensities were determined, indicative of the mean surface antigen expression of the total platelet population...

show abstract

Flow Cytometric Detection of Activated Platelets in Pregnant Women Prior to the Development of Pre-Eclampsia

Cited by 103 publications

References 19 publications

Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome?

Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. One cause of defective endovascular invasion in this syndrome?

Hypertension in pregnancy

Extensive platelet activation in preeclampsia compared with normal pregnancy: Enhanced expression of cell adhesion molecules

Contact Info

Product

Resources

About