Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Formation of the Platelet Plug01:22

Formation of the Platelet Plug

10.7K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
10.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Crystallographically controlled alignment of melt inclusion entrapment in magmatic olivine: Insights from Lab-Diffraction Contrast Tomography.

Micron (Oxford, England : 1993)·2026
Same author

Phages for One Health: regulatory and product life cycle considerations.

Microbiology (Reading, England)·2026
Same author

Survival and patient-reported outcomes of robotic arm-assisted patellofemoral arthroplasty and patient-acceptable symptom state thresholds : a multicentre retrospective cohort study with minimum one-year follow-up.

The bone & joint journal·2026
Same author

Surgical fixation versus non-surgical care for children with a displaced medial epicondyle fracture of the elbow (the SCIENCE study): a multicentre, randomised controlled, superiority trial and economic evaluation.

Lancet (London, England)·2026
Same author

Recombinant von Willebrand Factor (vonicog alfa) reduces platelet inhibition caused by antiplatelet drugs and has potential as an acute haemostatic agent.

Haematologica·2026
Same author

Postoperative outcomes based on timing of definitive fixation and flap coverage in Gustilo-Anderson 3B open tibia fractures.

Injury·2026

Related Experiment Video

Updated: Mar 30, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
05:31

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

1.5K

Syncytiotrophoblast Extracellular Vesicles from Pre-Eclampsia Placentas Differentially Affect Platelet Function.

Dionne S Tannetta1, Kathryn Hunt1, Chris I Jones2

  • 1Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Level 3, Women's Centre, John Radcliffe Hospital, Oxford, United Kingdom.

Plos One
|November 10, 2015
PubMed
Summary

Syncytiotrophoblast extracellular vesicles (STBEV) from the placenta activate platelets, with increased activation seen in pre-eclampsia (PE). Aspirin inhibits this STBEV-induced platelet aggregation, linking placental dysfunction to clotting risks in PE.

More Related Videos

siRNA Transfection and EMSA Analyses on Freshly Isolated Human Villous Cytotrophoblasts
09:57

siRNA Transfection and EMSA Analyses on Freshly Isolated Human Villous Cytotrophoblasts

Published on: September 20, 2016

11.2K
Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis
05:30

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

Published on: November 8, 2024

1.0K

Related Experiment Videos

Last Updated: Mar 30, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
05:31

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles

Published on: January 26, 2024

1.5K
siRNA Transfection and EMSA Analyses on Freshly Isolated Human Villous Cytotrophoblasts
09:57

siRNA Transfection and EMSA Analyses on Freshly Isolated Human Villous Cytotrophoblasts

Published on: September 20, 2016

11.2K
Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis
05:30

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis

Published on: November 8, 2024

1.0K

Area of Science:

  • Obstetrics and Gynecology
  • Maternal-Fetal Medicine
  • Cardiovascular Disease Research

Background:

  • Pre-eclampsia (PE) is a major cause of maternal mortality, characterized by hypertension and proteinuria.
  • PE pathophysiology involves placental dysfunction, leading to maternal systemic inflammation and hypercoagulation.
  • Women with PE have a higher risk of future cardiovascular disease.

Purpose of the Study:

  • To investigate the interaction between placental extracellular vesicles and maternal platelets in pre-eclampsia.
  • To determine if syncytiotrophoblast extracellular vesicles (STBEV) from PE placentas activate platelets.
  • To assess the effect of aspirin on STBEV-induced platelet activation.

Main Methods:

  • Isolation of STBEV from normal and PE placentas using ex vivo dual placental perfusion.
  • Incubation of isolated STBEV with platelets to assess platelet association and activation.
  • Treatment of platelets with aspirin to evaluate inhibition of STBEV-induced aggregation.

Main Results:

  • STBEV rapidly associate with platelets.
  • STBEV from normal placentas induce platelet activation, which is enhanced by STBEV from PE placentas.
  • Aspirin treatment inhibits STBEV-induced reversible platelet aggregation.

Conclusions:

  • STBEV play a role in platelet activation and aggregation in pre-eclampsia.
  • This interaction establishes a potential link between placental dysfunction and the hypercoagulable state in PE.
  • Findings suggest a mechanism contributing to the increased thrombotic risk in women with pre-eclampsia.