Syncytiotrophoblast Extracellular Vesicles from Pre-Eclampsia Placentas Differentially Affect Platelet Function
| Autor: | Tannetta, DS, Hunt, K, Jones, CI, Davidson, N, Coxon, CH, Ferguson, D, Redman, CW, Gibbins, JM, Sargent, IL, Tucker, KL, Oudejans, C |
|---|---|
| Přispěvatelé: | Oudejans, C |
| Rok vydání: | 2015 |
| Předmět: |
Adult
Blood Platelets medicine.medical_specialty Platelet Aggregation Placenta lcsh:Medicine 030204 cardiovascular system & hematology Biology Systemic inflammation 03 medical and health sciences Extracellular Vesicles 0302 clinical medicine Syncytiotrophoblast Microscopy Electron Transmission Pre-Eclampsia Pregnancy Internal medicine medicine Humans Platelet Platelet activation lcsh:Science 030304 developmental biology 0303 health sciences Aspirin Multidisciplinary Eclampsia lcsh:R Thrombosis medicine.disease Platelet Activation Pathophysiology 3. Good health Trophoblasts Endocrinology medicine.anatomical_structure Case-Control Studies embryonic structures lcsh:Q Female medicine.symptom medicine.drug Research Article |
| Zdroj: | PLoS ONE PLoS ONE, Vol 10, Iss 11, p e0142538 (2015) |
| ISSN: | 1932-6203 |
| Popis: | Pre-eclampsia (PE) complicates around 3% of all pregnancies and is one of the most common causes of maternal mortality worldwide. The pathophysiology of PE remains unclear however its underlying cause originates from the placenta and manifests as raised blood pressure, proteinuria, vascular or systemic inflammation and hypercoagulation in the mother. Women who develop PE are also at significantly higher risk of subsequently developing cardiovascular (CV) disease. In PE, the failing endoplasmic reticulum, oxidative and inflammatory stressed syncytiotrophoblast layer of the placenta sheds increased numbers of syncytiotrophoblast extracellular vesicles (STBEV) into the maternal circulation. Platelet reactivity, size and concentration are also known to be altered in some women who develop PE, although the underlying reasons for this have not been determined. In this study we show that STBEV from disease free placenta isolated ex vivo by dual placental perfusion associate rapidly with platelets. We provide evidence that STBEV isolated from normal placentas cause platelet activation and that this is increased with STBEV from PE pregnancies. Furthermore, treatment of platelets with aspirin, currently prescribed for women at high risk of PE to reduce platelet aggregation, also inhibits STBEV-induced reversible aggregation of washed platelets. Increased platelet reactivity as a result of exposure to PE placenta derived STBEVs correlates with increased thrombotic risk associated with PE. These observations establish a possible direct link between the clotting disturbances of PE and dysfunction of the placenta, as well as the known increased risk of thromboembolism associated with this condition. |
| Databáze: | OpenAIRE |
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