Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...

Formation of the Platelet Plug

Formation of the Platelet Plug

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...

Mechanism of Angiogenesis

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...

You might also read

Related Articles

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

Sort by

Same author

Targeting endothelial to mesenchymal transition in atherosclerosis.

Cardiovascular research·2026

Same author

Hypertension in autoimmune rheumatic diseases: a position paper from the European Society of Hypertension working group on small arteries. Part A: pathophysiology, prevalence and cardiovascular risk estimation.

Journal of hypertension·2026

Same author

Hypertension in autoimmune rheumatic diseases - a position paper from the European Society of Hypertension working group on small arteries. Part B: Recommendations for the clinical management of hypertension.

Journal of hypertension·2026

Same author

Country-specific prevalence and clinical relevance of elevated Lp(a) as a risk enhancer in 2 Greek cohorts.

Journal of clinical lipidology·2026

Same author

Amyloid-beta (1-40) peptide is associated with systemic metabolic health.

European journal of clinical investigation·2026

Same author

The complement-dendritic cell-endothelial cell crosstalk in vascular inflammation.

Cardiovascular research·2025

Same journal

Comparative Visual Outcomes of Toric and Nontoric Intraocular Lenses Featuring Combined Diffractive Extended Depth of Focus and Multifocal Designs.

Journal of ophthalmology·2026

Same journal

Prognostic Value of Interocular Flicker ERG Asymmetry in Acute Postoperative Endophthalmitis After Intraocular Surgery: A Pilot Study.

Journal of ophthalmology·2026

Same journal

Clinical Ophthalmology Consultations in Paediatric Inpatient Rehabilitation-A Retrospective Case-Note Analysis.

Journal of ophthalmology·2026

Same journal

Pathogenesis of Neovascular Glaucoma in Diabetic Retinopathy: A Review.

Journal of ophthalmology·2026

Same journal

Mathematical Modeling of IOL Power Changes After Pupil Dilation Based on Multifactorial Analysis.

Journal of ophthalmology·2026

Same journal

Reduced Neutrophil-to-Eosinophil Ratio in Chronic Dacryocystitis: A Hematological Clue to Allergic Pathogenesis.

Journal of ophthalmology·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Oct 30, 2025

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

Human Platelets Take up Anti-VEGF Agents.

B Sobolewska¹, B Fehrenbacher², P Münzer³

¹Center for Ophthalmology, Eberhard Karls University Tuebingen, Tuebingen, Germany.

Journal of Ophthalmology

|July 5, 2021

Summary

This summary is machine-generated.

Platelets internalize anti-vascular endothelial growth factor (anti-VEGF) agents, potentially increasing local anti-VEGF exposure and contributing to thromboembolic events. Different transport mechanisms for bevacizumab versus ranibizumab and aflibercept were observed.

More Related Videos

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

Published on: November 8, 2024

Decellularization and Recellularization Methodology for Human Saphenous Veins

Decellularization and Recellularization Methodology for Human Saphenous Veins

Published on: July 27, 2018

Related Experiment Videos

Last Updated: Oct 30, 2025

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors

Published on: March 15, 2016

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

An In Vitro Assay to Study Platelet Migration Using RGD-Functionalized Avidin-Biotin Tethers

Published on: November 8, 2024

Decellularization and Recellularization Methodology for Human Saphenous Veins

Decellularization and Recellularization Methodology for Human Saphenous Veins

Published on: July 27, 2018

Area of Science:

Ophthalmology
Hematology
Pharmacology

Background:

Repeated intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents lead to systemic exposure.
Anti-VEGF agents can penetrate the vascular barrier, raising questions about their interaction with non-resident platelets.

Purpose of the Study:

To investigate whether platelets uptake anti-VEGF agents (ranibizumab, aflibercept, bevacizumab) using visualization techniques.
To understand the interaction between platelets and systemically available anti-VEGF agents.

Main Methods:

Immunofluorescence and immunogold staining were used to examine anti-VEGF uptake in human platelets.
The roles of actin filaments and clathrin-coated vesicles in anti-VEGF transport were assessed using staurosporine and cytochalasin D inhibitors.

Main Results:

All three anti-VEGF agents (ranibizumab, aflibercept, bevacizumab) were internalized by platelets and colocalized with VEGF.
Ranibizumab and aflibercept primarily localized to alpha-granules, while bevacizumab was found in both alpha-granules and platelet vesicles.
Staurosporine and cytochalasin D inhibited aflibercept uptake and reduced ranibizumab and bevacizumab transport, with bevacizumab showing greater colocalization in clathrin-coated vesicles.

Conclusions:

Platelet uptake and alpha-granule internalization of anti-VEGF agents may increase local anti-VEGF exposure upon platelet activation, potentially contributing to arterial thromboembolic events.
Clathrin-coated vesicles appear more involved in bevacizumab transport compared to ranibizumab and aflibercept.
Further research is needed to determine if observed differences in bevacizumab localization and transport relate to specific receptor-mediated endocytosis mechanisms.